Oxidative Medicine and Cellular Longevity

Oxidative Medicine and Cellular Longevity / 2021 / Article
Special Issue

Effects of Plant-Based Compounds on Cellular and Molecular Mechanisms of Oxidative Stress

View this Special Issue

Review Article | Open Access

Volume 2021 |Article ID 3617498 | https://doi.org/10.1155/2021/3617498

Bo Liang, Yong-Chun Zhu, Jia Lu, Ning Gu, "Effects of Traditional Chinese Medication-Based Bioactive Compounds on Cellular and Molecular Mechanisms of Oxidative Stress", Oxidative Medicine and Cellular Longevity, vol. 2021, Article ID 3617498, 9 pages, 2021. https://doi.org/10.1155/2021/3617498

Effects of Traditional Chinese Medication-Based Bioactive Compounds on Cellular and Molecular Mechanisms of Oxidative Stress

Academic Editor: Marcio Carocho
Received18 Jul 2020
Accepted28 Apr 2021
Published14 May 2021

Abstract

The oxidative stress reaction is the imbalance between oxidation and antioxidation in the body, resulting in excessive production of oxygen free radicals in the body that cannot be removed, leading to excessive oxidation of the body, and causing damage to cells and tissues. A large number of studies have shown that oxidative stress is involved in the pathological process of many diseases, so inhibiting oxidative stress, that is, antioxidation, is of great significance for the treatment of diseases. Studies have shown that many traditional Chinese medications contain antioxidant active bioactive compounds, but the mechanisms of those compounds are different and complicated. Therefore, by summarizing the literature on antioxidant activity of traditional Chinese medication-based bioactive compounds in recent years, our review systematically elaborates the main antioxidant bioactive compounds contained in traditional Chinese medication and their mechanisms, so as to provide references for the subsequent research.

1. Introduction

Oxidative stress is the imbalance between oxidation and antioxidation in the body, which leads to the excessive production of oxygen free radicals that cannot be removed, resulting in excessive oxidation and thereby causing damage to cells and tissues [13]. Free radicals are also produced in a normal physiological state, but there are two kinds of antioxidant systems in our body: enzyme antioxidant system and nonenzymatic antioxidant system [4]. They clear free radicals produced by normal metabolism in the body to maintain the dynamic balance of free radical production and clearance and protect the body from oxidative damage. When the body is damaged exogenously or endogenously, the oxidation capacity of the body is enhanced, producing excessive free radicals and releasing a large number of reactive oxygen species (ROS). However, the reduction of antioxidant capacity makes the accumulation of excessive free radicals in the body cannot be removed, thus causing oxidative damage to the body and the occurrence of diseases [4]. Modern studies have shown that many traditional Chinese medications (TCM) and their bioactive compounds are rich in antioxidants, mainly including flavonoids, phenols, terpenes, polysaccharides, saponins, alkaloids, vitamins, and trace elements [5, 6]. Through their direct or indirect effects on the body’s antioxidant system, they achieve the purpose of eliminating excessive free radicals and thus protect the body [6]. Here, we summarize these recent advances in the field of TCM-based bioactive compounds as they apply to oxidative stress. In addition, current barriers for further research are also discussed. Due to the ongoing research in this field, we believe that stronger evidence to support the application of TCM-based bioactive compounds for oxidative stress will emerge in the near future.

2. TCM-Based Bioactive Compounds and Oxidative Stress

2.1. Polyphenols

Many TCM contain polyphenols, and their antioxidant mechanism is mainly related to the hydrogen donor of their phenolic hydroxyl groups, which can bind to free radicals and terminate the chain reaction of free radicals [79].

As natural polyphenolic phytochemicals that exist primarily in tea, tea polyphenols have been shown to have many clinical applications [10, 11]. Tea polyphenols could protect tri-ortho-cresyl phosphate-induced ovarian damage via inhibiting oxidative stress [12] and ameliorate hepatic oxidative stress though reducing hepatic inflammation and NLRP3 inflammasome activation caused by a moderate dose of perfluorodecanoic acid [13]. Additionally, it can not only regulate the antioxidant enzyme system in the body and play an efficient scavenging effect on free radicals by activating the Nrf2/Keap1 pathway [9, 14] but also inhibit the oxidase system in the body, such as inhibiting the production of NADPH oxidase, to reduce the production of ROS in vascular endothelium and protect the heart [9, 15]. Additionally, tea polyphenols could protect PC12 cells against methamphetamine-induced reactive oxide species production through increasing the antioxidant capacities and expressions of the phosphorylation of ataxia telangiectasia mutant and checkpoint kinase 2 [16]. Tea polyphenols decrease intracellular reactive oxygen species accumulation via activating NFE2L2 and MAPK pathways in bovine mammary epithelial cells exposed to hydrogen peroxides [17]. Fresh tea leaf is unusually rich in polyphenols known as catechins which may constitute up to 30% of the dry leaf weight [18]. Catechins are ROS scavengers and metal ion chelators, whereas their indirect antioxidant activities comprise induction of antioxidant enzymes, inhibition of prooxidant enzymes, and production of the phase II detoxification enzymes and antioxidant enzymes [19]. In a paralleled, crossover, and randomized controlled study, single-dose consumption of green tea catechins influences oxidative stress biomarkers, which could be beneficial for oxidative metabolism at rest and during exercise, possibly through the catechol-O-methyltransferase mechanism [20].

Salvianolic acid is another activity of phenolic acids. Salvianolic acid A/B/C are bioactive polyphenols extracted from Radix Salviae (Danshen), which possesses a variety of pharmacological activities. Salvianolic acid A effectively protects the kidney against oxidative stress in 5/6 nephrectomized rats by activating the Akt/GSK-3β/Nrf2 signaling pathway and inhibiting the NF-κB signaling pathway [21]. Salvianolic acid A ameliorates oxidation in ischemia-reperfusion-induced injury, and these protective effects may partially occur via activation of Nrf2/HO-1 and Akt/mTORC1 signaling pathways [22, 23]. Salvianolic acid A prevents Ang II-induced oxidative stress by inhibiting the activation of the Akt pathway in the macrophages [24]. Salvianolic acid B abolishes oxidative stress in the hippocampus by inhibiting NLRP3 inflammasome activation [25]. Salvianolic acid B protects the endothelial cells against oxidative stress injury by inhibiting endothelial permeability and MAPK and NF-κB signaling pathways [26]. Salvianolic acid B relieves oxidative stress via inhibiting the transforming growth factor-β1 pathway in lipopolysaccharide-induced acute lung injury rats [27]. Salvianolic acid B protects against subarachnoid hemorrhage-triggered oxidative damage by upregulating the Nrf2 antioxidant signaling pathway, which may be modulated by SIRT1 activation [28]. Furthermore, salvianolic acid C protects the hepatocytes from acetaminophen-induced oxidative stress damage by mitigating mitochondrial oxidative stress through inhibition of the Keap1/Nrf2/HO-1 signaling axis [29]. Salvianolic acid C effectively attenuates lipopolysaccharide-induced oxidative stress via the TLR4/NF-κB pathway [30].

The antioxidative effect of resveratrol in vivo is not to scavenge ROC directly but to play a role as a gene regulator [3133]. Resveratrol inhibits NADPH oxidase-mediated production of ROS by downregulating the expression and activity of the oxidase [31]. Resveratrol can activate SIRT1 [34]. Studies have shown that among the established SIRT1 targets, FoxO transcription factors contribute to the antioxidative effects of resveratrol by upregulating antioxidative enzymes and eNOS [31, 34, 35]. SIRT1 inhibits the production of ROS in mitochondria through proliferator-activated receptor-coactivator-1α deacetylation and nitric oxide-dependent mechanism [36]. Resveratrol results in relieving oxidative stress, which may be largely associated with the alleviation of metabolic disturbances [37]. In addition, resveratrol upregulated the activities of some antioxidant enzymes by activating Nrf2 [31, 38]. Resveratrol also has effects on nonenzymatic antioxidants [31]. For example, resveratrol can upregulate γ-glutamylcysteine synthetase by activating Nrf2 [38], thus increasing the content of glutathione in endothelial cells [39].

Polyphenols include also flavonoids, which are a series of compounds with C6-C3-C6 as the basic carbon frame [40, 41]. Their antioxidant and anti-inflammatory activities are mainly due to their ability to prevent or inhibit reactions related to oxygen free radicals, mediate or increase the activity of antioxidant enzymes, and thus scavenging ROS [2]. They can improve the antioxidant status by weakening the activity of the NF-κB pathway and inhibiting the expression of a variety of inflammatory cytokines and chemokines, such as monocyte chemoattractant protein-1, nitric oxide synthase, cyclooxygenase, lipoxygenase, cell adhesion molecules, tumor necrosis factor, and interleukin [2, 42].

Baicalein, a widely distributed natural flavonoid [43], downregulates protein kinase R-like ER kinase and upregulates Nrf2 to significantly alleviate oxidative stress [4447]. Moreover, baicalein exerts a protective effect under oxidative stress through regulating the KLF4/MARCH5/Drp1 pathway [48, 49], stabilizing carboxyl terminus of Hsc70-interacting protein activity to promote receptor-interacting serine/threonine kinase 1/3 ubiquitination and degradation [50], and regulating PARP-1/AIF [51] and NF-κB pathways [47, 52].

Baicalin, also extracted from Scutellariae Radix (Huangqin) [53, 54], alleviates intestinal oxidative damage by inhibiting NF-κB and increasing mTOR signaling to modulate downstream oxidative responses after deoxynivalenol challenge [55, 56]. Baicalin inactivates succinate dehydrogenase to suppress ROS production and protects glutamine synthetase protein stability against oxidative stress [57]. Baicalin treatment inhibits the NF-κB and p38 MAPK signaling pathways, thereby achieving its antioxidant effect in a dose-dependent manner in atherosclerosis [58]. Baicalin also protects against LPS-induced injury by decreasing oxidative stress [59] and represses C/EBPβ via redox homeostasis [60].

Luteolin is a common flavonoid that is abundantly present in various edible plants; it is known to exhibit beneficial effects [61]. Luteolin effectively alleviates oxidative stress injury induced by hydrogen peroxide through P38 MAPK/NF-κB activation [42, 6264]. Luteolin activates the Nrf2 pathway and increases the antioxidant defense capacities of ochratoxin A-treated cells [65]. Luteolin exhibits antioxidative property in lipopolysaccharide-stimulated murine macrophages through transforming growth factor beta-activated kinase 1 TAK1 inhibition and Nrf2 activation [66]. Luteolin also enhances the antioxidative process in intracerebral hemorrhage and testicular injury by activating the p62-Keap1-Nrf2 [67] or Nrf2/HO-1 pathway [68]. Moreover, p21 upregulation and mTOR signaling inhibition are involved in the antioxidant effect of luteolin [69].

The antioxidation of quercetin is mainly the result of the joint action of the catechol group on the B ring and the free hydroxyl group (OH-) on the A ring [70, 71]. In addition, quercetin has a 3-OH group, which is an effective inhibitor of lipid oxidation and can effectively reduce the abnormal production of ROS [42, 70]. Quercetin attenuates d-galactose-induced aging-related oxidative alterations through NF-κB [72], reverses lipopolysaccharide or 1,2-dimethylhydrazine-mediated oxidative stress via targeting the MAPK/Nrf2/Keap1 signaling pathway [73, 74], and improves d-galactosamine-induced cellular damage by inhibiting oxidative stress via inhibiting HMGB1 [75] and SIRT1/ER stress [76].

Silymarin can increase the activity of antioxidant enzymes, such as superoxide dismutase and catalase, so it can scavenge free radicals efficiently. Silymarin can also inhibit lipid peroxidation, so it can protect the integrity of the structure and function of hepatocytes from various oxidative damage [77, 78].

Puerarin prominently alleviated oxidative stress through TLR4/NLRP3 inflammasome activation [79], Nrf2 pathway [80, 81], and antioxidant enzymes [80] by significantly downregulating HIF-1α and upregulating TIMP-3 and BCL-2 [82]. Moreover, puerarin may inhibit MAPK and active STAT3 to enhance the antioxidant capacity [83].

2.2. Saponins

The main saponins in TCM are steroidal saponins and triterpenoid saponins. The contents of steroidal saponins were more in Anemarrhenae Rhizoma (Zhimu), Asparagi Radix (Tiandong), Ophiopogonis Radix (Maidong), and Paris polyphylla (Chonglou), and the contents of triterpenoid saponins in Panax ginseng C.A. Mey (Renshen), Acanthopanax senticosus (Rupr. Maxim.) Harms (Ciwujia), and Cimicifugae Rhizoma (Shengma) were higher.

The levels of malondialdehyde and lactate dehydrogenase can be reduced by timosaponin, which improves superoxide dismutase and nitric oxide [84]. The research showed that timosaponin could protect PC12 cells by reducing the level of ROS induced by hydrogen peroxide [85]. Timosaponin may have the effect of protecting INS-1 pancreatic β cells through reducing IL-1β production by inhibiting the NLRP3 inflammasome in macrophages and restoring the insulin secretion ability and cell viability by reducing oxidative stress [86]. Timosaponin can also reduce the activity of NF-κB to inhibit the production of inflammatory factors and reduce the inflammatory response [84].

Ginsenoside, a potential treatment candidate for the attenuation of aging-related disease [87], produces antidepressant-like effects on chronic unpredictable mild stress-exposed rats involving protection against oxidative stress and thus the neuronal deterioration resulting from inflammatory responses [88]. Ginsenoside not only upregulates GPX4 to reduce oxidative stress and thereby alleviates 6-hydroxydopamine-induced neuronal damage [89] but also effectively attenuates D-galactose-induced oxidative stress via restoring the upstream PI3K/AKT signaling pathway [90]. Besides, ginsenoside significantly ameliorates oxidative stress through regulating SIRT1 [91]. In cardiomyocytes, ginsenoside decreases oxidative stress via activating the antioxidant signal pathway of AMPK [92, 93], PERK/Nrf2/HMOX1 [94], and Nrf2 pathways [95, 96].

2.3. Polysaccharides

Polysaccharides are a kind of compound composed of more than 10 glycosyl groups bound by glycosidic bonds, which is one of the four basic substances of life [97]. Polysaccharides have the characteristic of antioxidant stress. Several antioxidant mechanisms of polysaccharides include direct scavenging of ROS, enhancement of antioxidant enzyme activity, and binding of polysaccharide molecules with metal ions necessary for ROS to inhibit the production of free radicals [98100].

Astragalus polysaccharides extracted from the dried rhizome of Astragalus membranaceus (Huangqi) can improve the activity of antioxidant enzymes and reduce oxidative stress indices [97, 101103]; it alleviates hydrogen peroxide-triggered oxidative injury via elevating the expression of KLF2 via the MEK/ERK pathway [104] and alleviates tilmicosin-induced toxicity by inhibiting oxidative damage and modulating the expressions of HSP70, NF-κB, and Nrf2/HO-1 pathway [105]. Astragalus polysaccharides can also effectively alleviate oxidative stress-mediated osteoporosis, which may be related to its regulation of the FoxO3a/Wnt2/β-catenin pathway [106]. Astragalus polysaccharides combined with matrine exert a synergistic protective effect against oxidative stress, which might be associated with regulating TFF3 expression [107].

Lycium barbarum polysaccharides from Goji berries or Lycium barbarum L. (Gouqi) could protect retinal ganglion cells from CoCl2-induced apoptosis by reducing mitochondrial membrane potential and ROC [108]. And Lycium barbarum polysaccharides present antioxidant effects with utility [109, 110], resulting from direct reduction of ROS, restoration of endogenous antioxidant enzymes, and downregulation of p-eIF2α, GRP78, and CHOP [97, 101, 110, 111].

Ziziphus jujuba polysaccharides from Ziziphus jujuba Mill (Zao) contain four fractions (one neutral polysaccharide fraction named ZJPN and three acidic polysaccharide fractions named ZJPa1, ZJPa2, and ZJPa3 separately), and their superoxide anion scavenging ability is stronger than hydroxyl radicals [112]. In addition, the acidic polysaccharide fractions show outstanding chelation to ferrous ions [101].

Other polysaccharides such as Angelica polysaccharides can increase the activity of superoxide dismutase, reduce the level of malondialdehyde, and overenhance the phosphorylation of Akt/hTERT to mitigate the harm of the peroxidation of low-density lipoprotein [113, 114]. Further, Angelica polysaccharides can upregulate miR-126, which could activate the PI3K/AKT and mTOR signal pathways, to attenuate cellular oxidative response damage [115].

Cordyceps (Dongchongxiacao) is a genus of ascomycete fungi that has been used for TCM [116]. The polysaccharides contained in Cordyceps have a good ability to scavenge DPPH and ABTS free radicals [101, 117].

3. Conclusions

Many TCM-based bioactive compounds are rich in antioxidants and have good development prospects. However, different bioactive compounds have different targets for inhibiting oxidative stress (see Table 1), and the side effects of various bioactive compounds have not been fully studied. Therefore, we need to further explore the antioxidant mechanisms of TCM and in-depth study the side effects of related bioactive compounds to provide protection for the treatment of related diseases.


Bioactive compoundsCellular and molecular mechanismsReferences

Polyphenols
 Tea polyphenolsReduce inflammation and NLRP3 inflammasome activation, regulate the antioxidant enzyme system and play an efficient scavenging effect on free radicals by activating the Nrf2/Keap1 pathway, inhibit the oxidase system, increase the antioxidant capacities and expressions of p-ATM and p-Chk2, and activate NFE2L2 and MAPK pathways.[9, 1217]
 Salvianolic acidRegulate Akt, Keap1/Nrf2/HO-1, TLR4/NF-κB, and MAPK signaling pathways, inhibit NLRP3 inflammasome activation, inhibit endothelial permeability, and inhibit transforming growth factor-β1 pathway.[2130]
 ResveratrolInhibit NADPH oxidase-mediated production, activate SIRT1, upregulate antioxidative enzymes and eNOS, alleviate metabolic disturbances, upregulate the activities of some antioxidant enzymes by activating Nrf2, and upregulate γ-glutamylcysteine synthetase by activating Nrf2.[31, 3439]
 BaicaleinDownregulate PERK and upregulate Nrf2; regulate KLF4-MARCH5-Drp1, PARP-1/AIF, and NF-κB pathways; and stabilize CHIP activity to promote RIPK1/RIPK3 ubiquitination and degradation.[4452]
 BaicalinInhibit NF-κB and p38 MAPK signaling pathways and increase mTOR signaling, inactivate succinate dehydrogenase to suppress ROS production, and repress C/EBPβ via redox homeostasis.[5560]
 LuteolinActivate P38 MAPK/NF-κB, Nrf2, and p21 pathways; inhibit mTOR signaling.[42, 6269]
 QuercetinAttenuate oxidative alterations through NF-κB and MAPK/Nrf2/Keap1 signaling pathways; inhibit HMGB1 and SIRT1/ER stress.[7276]
 SilymarinIncrease the activity of antioxidant enzymes; inhibit lipid peroxidation.[77, 78]
 PuerarinAlleviate oxidative stress through TLR4/NLRP3 inflammasome activation, Nrf2 pathway, and antioxidant enzymes by downregulating HIF-1α and upregulating TIMP-3 and BCL-2; inhibit MAPK and active STAT3.[7983]
Saponins
 TimosaponinReduce MDA and LDH, improve SOD and NO, reduce ROS, reduce IL-1β production by inhibiting the NLRP3 inflammasome, and reduce the activity of NF-κB.[8486]
 GinsenosideUpregulate GPX4; restore the PI3K/AKT signaling pathway; regulate SIRT1; and activate AMPK, PERK/Nrf2/HMOX1, and Nrf2 pathways.[8896]
Polysaccharides
 Astragalus polysaccharidesImprove the activity of antioxidant enzymes and reduce oxidative stress indices; alleviate oxidative injury via elevating the expression of KLF2 via the MEK/ERK pathway; inhibit oxidative damage and modulate the expressions of HSP70, NF-κB, and Nrf2/HO-1 pathway; and regulate FoxO3a/Wnt2/β-catenin pathway.[97, 101106]
 Lycium barbarum polysaccharidesReduce mitochondrial membrane potential and ROC, reduce ROS, restore endogenous antioxidant enzymes, and downregulate p-eIF2α, GRP78, and CHOP.[97, 101, 108111]
 Ziziphus jujuba polysaccharidesStrong superoxide anion scavenging ability; outstanding chelation to ferrous ions.[101, 112]
 Angelica polysaccharidesIncrease SOD, reduce MDA, and overenhance the phosphorylation of Akt/hTERT; upregulate mir-126, which could activate the PI3K/AKT and mTOR signal pathways.[113115]
 Cordyceps polysaccharidesGood ability of scavenging DPPH and ABTS free radicals.[101]

Data Availability

The data used to support the findings of this study are included within the article.

Conflicts of Interest

The authors declare that there is no conflict of interest regarding the publication of this paper.

Acknowledgments

We thank all individuals involved in oxidative stress and TCM. This work was supported by the National Natural Science Foundation of China (81774229); Research and Practice Innovation Plan for Postgraduates of Jiangsu, China; Jiangsu Leading Talent Project of Traditional Chinese Medicine (Jiangsu TCM 2018 No. 4); Major Project of Nanjing Medical Science and Technology Development During 13th Five-year Plan (ZDX16013); and Jiangsu Universities Nursing Advantage Discipline Project (2019YSHL095).

References

  1. H. Sies, “Oxidative stress: a concept in redox biology and medicine,” Redox Biology., vol. 4, pp. 180–183, 2015. View at: Publisher Site | Google Scholar
  2. S. Das, I. Mitra, S. Batuta, M. Niharul Alam, K. Roy, and N. A. Begum, “Design, synthesis and exploring the quantitative structure-activity relationship of some antioxidant flavonoid analogues,” Bioorganic and Medicinal Chemistry Letters, vol. 24, no. 21, pp. 5050–5054, 2014. View at: Publisher Site | Google Scholar
  3. E. Zaplatic, M. Bule, S. Z. A. Shah, M. S. Uddin, and K. Niaz, “Molecular mechanisms underlying protective role of quercetin in attenuating Alzheimer's disease,” Life Sciences, vol. 224, pp. 109–119, 2019. View at: Publisher Site | Google Scholar
  4. S. Janciauskiene, “The beneficial effects of antioxidants in health and diseases,” Chronic Obstructive Pulmonary Diseases, vol. 7, no. 3, pp. 182–202, 2020. View at: Publisher Site | Google Scholar
  5. Y. Zhong, M. C. Menon, Y. Deng, Y. Chen, and J. C. He, “Recent advances in traditional Chinese medicine for kidney disease,” American Journal of Kidney Diseases, vol. 66, no. 3, pp. 513–522, 2015. View at: Publisher Site | Google Scholar
  6. B. Liang, Y. Zhou, L. Fu, and H. L. Liao, “Antiarrhythmic mechanisms of Chinese herbal medicine Dingji Fumai decoction,” Evidence-Based Complementary and Alternative Medicine, vol. 2020, Article ID 9185707, 9 pages, 2020. View at: Publisher Site | Google Scholar
  7. H. S. Oz, “Chronic inflammatory diseases and green tea polyphenols,” Nutrients, vol. 9, no. 6, p. 561, 2017. View at: Publisher Site | Google Scholar
  8. E. Roh, J.-E. Kim, J. Y. Kwon et al., “Molecular mechanisms of green tea polyphenols with protective effects against skin photoaging,” Critical Reviews in Food Science and Nutrition, vol. 57, no. 8, pp. 1631–1637, 2017. View at: Publisher Site | Google Scholar
  9. L. Xing, H. Zhang, R. Qi, R. Tsao, and Y. Mine, “Recent advances in the understanding of the health benefits and molecular mechanisms associated with green tea polyphenols,” Journal of Agricultural and Food Chemistry, vol. 67, no. 4, pp. 1029–1043, 2019. View at: Publisher Site | Google Scholar
  10. S.-T. Wang, W.-Q. Cui, D. Pan, M. Jiang, B. Chang, and L.-X. Sang, “Tea polyphenols and their chemopreventive and therapeutic effects on colorectal cancer,” World Journal of Gastroenterology, vol. 26, no. 6, pp. 562–597, 2020. View at: Publisher Site | Google Scholar
  11. M. Alagawany, M. E. Abd el-Hack, M. Saeed et al., “Nutritional applications and beneficial health applications of green tea and l‐theanine in some animal species: a review,” Journal of Animal Physiology and Animal Nutrition, vol. 104, no. 1, pp. 245–256, 2020. View at: Publisher Site | Google Scholar
  12. S. Yang, S. Shao, B. Huang et al., “Tea polyphenols alleviate tri‐ortho‐cresyl phosphate‐induced autophagy of mouse ovarian granulosa cells,” Environmental Toxicology, vol. 35, no. 4, pp. 478–486, 2020. View at: Publisher Site | Google Scholar
  13. D. Wang, Q. Gao, T. Wang et al., “Green tea polyphenols and epigallocatechin-3-gallate protect against perfluorodecanoic acid induced liver damage and inflammation in mice by inhibiting NLRP3 inflammasome activation,” Food Research International, vol. 127, p. 108628, 2020. View at: Publisher Site | Google Scholar
  14. M. C. Jaramillo and D. D. Zhang, “The emerging role of the Nrf2-Keap1 signaling pathway in cancer,” Genes and Development, vol. 27, no. 20, pp. 2179–2191, 2013. View at: Publisher Site | Google Scholar
  15. H.-S. Kim, M. J. Quon, and J.-a. Kim, “New insights into the mechanisms of polyphenols beyond antioxidant properties; lessons from the green tea polyphenol, epigallocatechin 3-gallate,” Redox Biology, vol. 2, pp. 187–195, 2014. View at: Publisher Site | Google Scholar
  16. Q. Ru, Q. Xiong, X. Tian et al., “Tea polyphenols attenuate methamphetamine-induced neuronal damage in PC12 cells by alleviating oxidative stress and promoting DNA repair,” Frontiers in Physiology, vol. 10, p. 1450, 2019. View at: Publisher Site | Google Scholar
  17. Y. Ma, L. Zhao, M. Gao, and J. J. Loor, “Tea polyphenols protect bovine mammary epithelial cells from hydrogen peroxide-induced oxidative damage in vitro1,” Journal of Animal Science, vol. 96, no. 10, pp. 4159–4172, 2018. View at: Publisher Site | Google Scholar
  18. H. N. Graham, “Green tea composition, consumption, and polyphenol chemistry,” Preventive Medicine, vol. 21, no. 3, pp. 334–350, 1992. View at: Publisher Site | Google Scholar
  19. J. Bernatoniene and D. Kopustinskiene, “The Role of Catechins in Cellular Responses to Oxidative Stress,” Molecules, vol. 23, no. 4, p. 965, 2018. View at: Publisher Site | Google Scholar
  20. M. Sugita, M. P. Kapoor, A. Nishimura, and T. Okubo, “Influence of green tea catechins on oxidative stress metabolites at rest and during exercise in healthy humans,” Nutrition, vol. 32, no. 3, pp. 321–331, 2016. View at: Publisher Site | Google Scholar
  21. H.-F. Zhang, J.-H. Wang, Y.-L. Wang et al., “Salvianolic Acid A Protects the Kidney against Oxidative Stress by Activating the Akt/GSK-3β/Nrf2 Signaling Pathway and Inhibiting the NF-κB Signaling Pathway in 5/6 Nephrectomized Rats,” Oxidative Medicine and Cellular Longevity, vol. 2019, Article ID 2853534, 16 pages, 2019. View at: Publisher Site | Google Scholar
  22. G. Zu, T. Zhou, N. Che, and X. Zhang, “Salvianolic acid A protects against oxidative stress and apoptosis induced by intestinal ischemia-reperfusion injury through activation of Nrf2/HO-1 pathways,” Cellular Physiology and Biochemistry., vol. 49, no. 6, pp. 2320–2332, 2018. View at: Publisher Site | Google Scholar
  23. H. Zhang, Y.-y. Liu, Q. Jiang et al., “Salvianolic acid A protects RPE cells against oxidative stress through activation of Nrf2/HO-1 signaling,” Free Radical Biology and Medicine, vol. 69, pp. 219–228, 2014. View at: Publisher Site | Google Scholar
  24. L. Li, T. Xu, Y. du et al., “Salvianolic acid A attenuates cell apoptosis, oxidative stress, Akt and NF-κB activation in angiotensin-II induced murine peritoneal macrophages,” Current Pharmaceutical Biotechnology, vol. 17, no. 3, pp. 283–290, 2016. View at: Publisher Site | Google Scholar
  25. Q. Huang, X. Ye, L. Wang, and J. Pan, “Salvianolic acid B abolished chronic mild stress-induced depression through suppressing oxidative stress and neuro-inflammation via regulating NLRP3 inflammasome activation,” Journal of Food Biochemistry, vol. 43, no. 3, article e12742, 2019. View at: Publisher Site | Google Scholar
  26. Q. Liu, X. Shi, L. Tang et al., “Salvianolic acid B attenuates experimental pulmonary inflammation by protecting endothelial cells against oxidative stress injury,” European Journal of Pharmacology, vol. 840, pp. 9–19, 2018. View at: Publisher Site | Google Scholar
  27. D.-H. Zhao, Y.-J. Wu, S.-T. Liu, and R.-Y. Liu, “Salvianolic acid B attenuates lipopolysaccharide-induced acute lung injury in rats through inhibition of apoptosis, oxidative stress and inflammation,” Experimental and Therapeutic Medicine, vol. 14, no. 1, pp. 759–764, 2017. View at: Publisher Site | Google Scholar
  28. X. Zhang, Q. Wu, Y. Lu et al., “Cerebroprotection by salvianolic acid B after experimental subarachnoid hemorrhage occurs via Nrf2- and SIRT1-dependent pathways,” Free Radical Biology and Medicine, vol. 124, pp. 504–516, 2018. View at: Publisher Site | Google Scholar
  29. C.-T. Wu, J.-S. Deng, W.-C. Huang, P.-C. Shieh, M.-I. Chung, and G.-J. Huang, “Salvianolic acid C against acetaminophen-induced acute liver injury by attenuating inflammation, oxidative stress, and apoptosis through inhibition of the Keap1/Nrf2/HO-1 signaling,” Oxidative Medicine and Cellular Longevity, vol. 2019, Article ID 9056845, 13 pages, 2019. View at: Publisher Site | Google Scholar
  30. Y. Duan, W. An, H. Wu, and Y. Wu, “Salvianolic acid C attenuates LPS-induced inflammation and apoptosis in human periodontal ligament stem cells via toll-like receptors 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway,” Medical Science Monitor, vol. 25, pp. 9499–9508, 2019. View at: Publisher Site | Google Scholar
  31. N. Xia, A. Daiber, U. Förstermann, and H. Li, “Antioxidant effects of resveratrol in the cardiovascular system,” British Journal of Pharmacology, vol. 174, no. 12, pp. 1633–1646, 2017. View at: Publisher Site | Google Scholar
  32. H. Li, N. Xia, and U. Förstermann, “Cardiovascular effects and molecular targets of resveratrol,” Nitric Oxide: Biology and Chemistry, vol. 26, no. 2, pp. 102–110, 2012. View at: Publisher Site | Google Scholar
  33. N. Xia, U. Forstermann, and H. Li, “Resveratrol as a gene regulator in the vasculature,” Current Pharmaceutical Biotechnology, vol. 15, no. 4, pp. 401–408, 2014. View at: Publisher Site | Google Scholar
  34. C.-P. Hsu, P. Zhai, T. Yamamoto et al., “Silent information regulator 1 protects the heart from ischemia/reperfusion,” Circulation, vol. 122, no. 21, pp. 2170–2182, 2010. View at: Publisher Site | Google Scholar
  35. K. Hasegawa, S. Wakino, K. Yoshioka et al., “Sirt1 protects against oxidative stress-induced renal tubular cell apoptosis by the bidirectional regulation of catalase expression,” Biochemical and Biophysical Research Communications, vol. 372, no. 1, pp. 51–56, 2008. View at: Publisher Site | Google Scholar
  36. C. Beauloye, L. Bertrand, S. Horman, and L. Hue, “AMPK activation, a preventive therapeutic target in the transition from cardiac injury to heart failure,” Cardiovascular Research, vol. 90, no. 2, pp. 224–233, 2011. View at: Publisher Site | Google Scholar
  37. K. Szkudelska, M. Okulicz, I. Hertig, and T. Szkudelski, “Resveratrol ameliorates inflammatory and oxidative stress in type 2 diabetic Goto-Kakizaki rats,” Biomedicine and Pharmacotherapy, vol. 125, p. 110026, 2020. View at: Publisher Site | Google Scholar
  38. Z. Ungvari, Z. Bagi, A. Feher et al., “Resveratrol confers endothelial protection via activation of the antioxidant transcription factor Nrf2,” American Journal of Physiology Heart and Circulatory Physiology, vol. 299, no. 1, pp. H18–H24, 2010. View at: Publisher Site | Google Scholar
  39. Z. Ungvari, N. Labinskyy, P. Mukhopadhyay et al., “Resveratrol attenuates mitochondrial oxidative stress in coronary arterial endothelial cells,” American Journal of Physiology Heart and Circulatory Physiology, vol. 297, no. 5, pp. H1876–H1881, 2009. View at: Publisher Site | Google Scholar
  40. T.-Y. Wang, Q. Li, and K.-S. Bi, “Bioactive flavonoids in medicinal plants: structure, activity and biological fate,” Asian Journal of Pharmaceutical Sciences, vol. 13, no. 1, pp. 12–23, 2018. View at: Publisher Site | Google Scholar
  41. M. Rodriguez-Canales, E. Martinez-Galero, A. D. Nava-Torres et al., “Anti-Inflammatory and Antioxidant Activities of the Methanolic Extract of Cyrtocarpa procera Bark Reduces the Severity of Ulcerative Colitis in a Chemically Induced Colitis Model,” Mediators of Inflammation, vol. 2020, Article ID 5062506, 11 pages, 2020. View at: Publisher Site | Google Scholar
  42. M. M. Fardoun, D. Maaliki, N. Halabi et al., “Flavonoids in adipose tissue inflammation and atherosclerosis: one arrow, two targets,” Clinical Science, vol. 134, no. 12, pp. 1403–1432, 2020. View at: Publisher Site | Google Scholar
  43. L. Avila-Carrasco, P. Majano, J. A. Sánchez-Toméro et al., “Natural plants compounds as modulators of epithelial-to-mesenchymal transition,” Frontiers in Pharmacology, vol. 10, p. 715, 2019. View at: Publisher Site | Google Scholar
  44. Y. Dong, Y. Xing, J. Sun, W. Sun, Y. Xu, and C. Quan, “Baicalein alleviates liver oxidative stress and apoptosis induced by high-level glucose through the activation of the PERK/Nrf2 signaling pathway,” Molecules, vol. 25, no. 3, p. 599, 2020. View at: Publisher Site | Google Scholar
  45. J. Ma, S. Li, L. Zhu et al., “Baicalein protects human vitiligo melanocytes from oxidative stress through activation of NF-E2-related factor2 (Nrf2) signaling pathway,” Free Radical Biology and Medicine, vol. 129, pp. 492–503, 2018. View at: Publisher Site | Google Scholar
  46. J. Y. Jeong, H.-J. Cha, E. O. Choi et al., “Activation of the Nrf2/HO-1 signaling pathway contributes to the protective effects of baicalein against oxidative stress-induced DNA damage and apoptosis in HEI193 Schwann cells,” International Journal of Medical Sciences, vol. 16, no. 1, pp. 145–155, 2019. View at: Publisher Site | Google Scholar
  47. Y. Yuan, W. Men, X. Shan et al., “Baicalein exerts neuroprotective effect against ischaemic/reperfusion injury via alteration of NF-kB and LOX and AMPK/Nrf2 pathway,” Inflammopharmacology, vol. 28, no. 5, pp. 1327–1341, 2020. View at: Publisher Site | Google Scholar
  48. Q. Li, Z. Yu, D. Xiao et al., “Baicalein inhibits mitochondrial apoptosis induced by oxidative stress in cardiomyocytes by stabilizing MARCH5 expression,” Journal of Cellular and Molecular Medicine, vol. 24, no. 2, pp. 2040–2051, 2020. View at: Publisher Site | Google Scholar
  49. Z. Yu, Q. Li, Y. Wang, and P. Li, “A potent protective effect of baicalein on liver injury by regulating mitochondria-related apoptosis,” Apoptosis, vol. 25, no. 5-6, pp. 412–425, 2020. View at: Publisher Site | Google Scholar
  50. Y. Wang, L. Li, G. Liu et al., “Baicalein protects cardiomyocytes from oxidative stress induced programmed necrosis by stabilizing carboxyl terminus of Hsc70-interacting protein,” International Journal of Cardiology, vol. 311, pp. 83–90, 2020. View at: Publisher Site | Google Scholar
  51. W.-H. Li, Y.-L. Yang, X. Cheng et al., “Baicalein attenuates caspase-independent cells death via inhibiting PARP-1 activation and AIF nuclear translocation in cerebral ischemia/reperfusion rats,” Apoptosis, vol. 25, no. 5-6, pp. 354–369, 2020. View at: Publisher Site | Google Scholar
  52. J.-J. Yan, G. H. du, X.-M. Qin, and L. Gao, “Baicalein attenuates the neuroinflammation in LPS-activated BV-2 microglial cells through suppression of pro-inflammatory cytokines, COX2/NF-κB expressions and regulation of metabolic abnormality,” International Immunopharmacology, vol. 79, p. 106092, 2020. View at: Publisher Site | Google Scholar
  53. P. Cheng, T. Wang, W. Li et al., “Baicalin alleviates lipopolysaccharide-induced liver inflammation in chicken by suppressing TLR4-mediated NF-κB pathway,” Frontiers in Pharmacology, vol. 8, p. 547, 2017. View at: Publisher Site | Google Scholar
  54. H. Chen, Y. He, S. Chen, S. Qi, and J. Shen, “Therapeutic targets of oxidative/nitrosative stress and neuroinflammation in ischemic stroke: applications for natural product efficacy with omics and systemic biology,” Pharmacological Research, vol. 158, p. 104877, 2020. View at: Publisher Site | Google Scholar
  55. P. Liao, Y. Li, M. Li et al., “Baicalin alleviates deoxynivalenol-induced intestinal inflammation and oxidative stress damage by inhibiting NF-κB and increasing mTOR signaling pathways in piglets,” Food and Chemical Toxicology, vol. 140, p. 111326, 2020. View at: Publisher Site | Google Scholar
  56. A. Zha, Z. Cui, M. Qi et al., “Dietary baicalin zinc supplementation alleviates oxidative stress and enhances nutrition absorption in deoxynivalenol challenged pigs,” Current Drug Metabolism, vol. 21, no. 8, pp. 614–625, 2020. View at: Publisher Site | Google Scholar
  57. X. Song, Z. Gong, K. Liu, J. Kou, B. Liu, and K. Liu, “Baicalin combats glutamate excitotoxicity via protecting glutamine synthetase from ROS-induced 20S proteasomal degradation,” Redox Biology, vol. 34, p. 101559, 2020. View at: Publisher Site | Google Scholar
  58. Y. Wu, F. Wang, L. Fan et al., “Baicalin alleviates atherosclerosis by relieving oxidative stress and inflammatory responses via inactivating the NF-κB and p38 MAPK signaling pathways,” Biomedicine and Pharmacotherapy, vol. 97, pp. 1673–1679, 2018. View at: Publisher Site | Google Scholar
  59. J. Ma, R. Wang, H. Yan, R. Xu, A. Xu, and J. Zhang, “Protective effects of Baicalin on lipopolysaccharide-induced injury in Caenorhabditis elegans,” Pharmacology, vol. 105, no. 1-2, pp. 109–117, 2020. View at: Publisher Site | Google Scholar
  60. K. Lei, Y. Shen, Y. He et al., “Baicalin Represses C/EBPβ via Its Antioxidative Effect in Parkinson’s Disease,” Oxidative Medicine and Cellular Longevity, vol. 2020, Article ID 8951907, 14 pages, 2020. View at: Publisher Site | Google Scholar
  61. T. Boeing, P. de Souza, S. Speca et al., “Luteolin prevents irinotecan‐induced intestinal mucositis in mice through antioxidant and anti‐inflammatory properties,” British Journal of Pharmacology., vol. 177, no. 10, pp. 2393–2408, 2020. View at: Publisher Site | Google Scholar
  62. H. I. Chen, W.-S. Hu, M.-Y. Hung et al., “Protective effects of luteolin against oxidative stress and mitochondrial dysfunction in endothelial cells,” Nutrition, Metabolism, and Cardiovascular Diseases, vol. 30, no. 6, pp. 1032–1043, 2020. View at: Publisher Site | Google Scholar
  63. W. Wu, D. Li, Y. Zong et al., “Luteolin inhibits inflammatory responses via p38/MK2/TTP-mediated mRNA stability,” Molecules, vol. 18, no. 7, pp. 8083–8094, 2013. View at: Publisher Site | Google Scholar
  64. M. Vatarescu, S. Bechor, Y. Haim et al., “Adipose tissue supports normalization of macrophage and liver lipid handling in obesity reversal,” The Journal of Endocrinology, vol. 233, no. 3, pp. 293–305, 2017. View at: Publisher Site | Google Scholar
  65. M. Liu, C. Cheng, X. Li et al., “Luteolin alleviates ochratoxin A induced oxidative stress by regulating Nrf2 and HIF-1α pathways in NRK-52E rat kidney cells,” Food and Chemical Toxicology, vol. 141, p. 111436, 2020. View at: Publisher Site | Google Scholar
  66. Y.-C. Cho, J. Park, and S. Cho, “Anti-inflammatory and anti-oxidative effects of luteolin-7-O-glucuronide in LPS-stimulated murine macrophages through TAK1 inhibition and Nrf2 activation,” International Journal of Molecular Sciences, vol. 21, no. 6, p. 2007, 2020. View at: Publisher Site | Google Scholar
  67. X. Tan, Y. Yang, J. Xu et al., “Luteolin exerts neuroprotection via modulation of the p62/Keap1/Nrf2 pathway in intracerebral hemorrhage,” Frontiers in Pharmacology, vol. 10, p. 1551, 2020. View at: Publisher Site | Google Scholar
  68. W. A. al-Megrin, S. Alomar, A. F. Alkhuriji et al., “Luteolin protects against testicular injury induced by lead acetate by activating the Nrf2/HO‐1 pathway,” IUBMB Life, vol. 72, no. 8, pp. 1787–1798, 2020. View at: Publisher Site | Google Scholar
  69. K. Iida, T. Naiki, A. Naiki-Ito et al., “Luteolin suppresses bladder cancer growth via regulation of mechanistic target of rapamycin pathway,” Cancer Science, vol. 111, no. 4, pp. 1165–1179, 2020. View at: Publisher Site | Google Scholar
  70. J. Mlcek, T. Jurikova, S. Skrovankova, and J. Sochor, “Quercetin and its anti-allergic immune response,” Molecules, vol. 21, no. 5, p. 623, 2016. View at: Publisher Site | Google Scholar
  71. L. Xiao, G. Luo, Y. Tang, and P. Yao, “Quercetin and iron metabolism: what we know and what we need to know,” Food and Chemical Toxicology, vol. 114, pp. 190–203, 2018. View at: Publisher Site | Google Scholar
  72. A. H. el-Far, M. A. Lebda, A. E. Noreldin et al., “Quercetin attenuates pancreatic and renal D-galactose-induced aging-related oxidative alterations in rats,” International Journal of Molecular Sciences, vol. 21, no. 12, p. 4348, 2020. View at: Publisher Site | Google Scholar
  73. L. Sun, G. Xu, Y. Dong, M. Li, L. Yang, and W. Lu, “Quercetin protects against lipopolysaccharide-induced intestinal oxidative stress in broiler chickens through activation of Nrf2 pathway,” Molecules, vol. 25, no. 5, p. 1053, 2020. View at: Publisher Site | Google Scholar
  74. S. G. Darband, S. Sadighparvar, B. Yousefi et al., “Quercetin attenuated oxidative DNA damage through NRF2 signaling pathway in rats with DMH induced colon carcinogenesis,” Life Sciences, vol. 253, p. 117584, 2020. View at: Publisher Site | Google Scholar
  75. P. Fang, J. Liang, X. Jiang et al., “Quercetin attenuates d-GaLN-induced L02 cell damage by suppressing oxidative stress and mitochondrial apoptosis via inhibition of HMGB1,” Frontiers in Pharmacology, vol. 11, p. 608, 2020. View at: Publisher Site | Google Scholar
  76. T. Hu, J.-J. Shi, J. Fang, Q. Wang, Y.-B. Chen, and S.-J. Zhang, “Quercetin ameliorates diabetic encephalopathy through SIRT1/ER stress pathway in db/db mice,” Aging, vol. 12, no. 8, pp. 7015–7029, 2020. View at: Publisher Site | Google Scholar
  77. S. Clichici, D. Olteanu, A. Filip, A.-L. Nagy, A. Oros, and P. A. Mircea, “Beneficial effects of silymarin after the discontinuation of CCl4-induced liver fibrosis,” Journal of Medicinal Food, vol. 19, no. 8, pp. 789–797, 2016. View at: Publisher Site | Google Scholar
  78. A. Tajmohammadi, B. M. Razavi, and H. Hosseinzadeh, “Silybum marianum(milk thistle) and its main constituent, silymarin, as a potential therapeutic plant in metabolic syndrome: a review,” Phytotherapy Research, vol. 32, no. 10, pp. 1933–1949, 2018. View at: Publisher Site | Google Scholar
  79. L. Guan, C. Li, Y. Zhang et al., “Puerarin ameliorates retinal ganglion cell damage induced by retinal ischemia/reperfusion through inhibiting the activation of TLR4/NLRP3 inflammasome,” Life Sciences, vol. 256, p. 117935, 2020. View at: Publisher Site | Google Scholar
  80. Y.-D. Jeon, J.-H. Lee, Y.-M. Lee, and D.-K. Kim, “Puerarin inhibits inflammation and oxidative stress in dextran sulfate sodium- induced colitis mice model,” Biomedicine and Pharmacotherapy, vol. 124, p. 109847, 2020. View at: Publisher Site | Google Scholar
  81. M. Li, D. Yuan, Y. Liu, H. Jin, and B. Tan, “Dietary Puerarin supplementation alleviates oxidative stress in the small intestines of Diquat-challenged piglets,” Animals, vol. 10, no. 4, p. 631, 2020. View at: Publisher Site | Google Scholar
  82. M. Waqas, H. Qamar, J. Zhang et al., “Puerarin enhance vascular proliferation and halt apoptosis in thiram-induced avian tibial dyschondroplasia by regulating HIF-1α, TIMP-3 and BCL-2 expressions,” Ecotoxicology and Environmental Safety, vol. 190, p. 110126, 2020. View at: Publisher Site | Google Scholar
  83. Q. Song, Y. Zhao, Q. Li, X. Han, and J. Duan, “Puerarin protects against iron overload-induced retinal injury through regulation of iron-handling proteins,” Biomedicine and Pharmacotherapy, vol. 122, p. 109690, 2020. View at: Publisher Site | Google Scholar
  84. Y.-L. Yuan, B.-Q. Lin, C.-F. Zhang et al., “Timosaponin B-II ameliorates palmitate-induced insulin resistance and inflammation via via IRS-1/PI3K/Akt and IKK/NF-κB Pathways,” The American Journal of Chinese Medicine, vol. 44, no. 4, pp. 755–769, 2016. View at: Publisher Site | Google Scholar
  85. Q. Xie, H. Zhao, N. Li, L. Su, X. Xu, and Z. Hong, “Protective effects of timosaponin BII on oxidative stress damage in PC12 cells based on metabolomics,” Biomedical Chromatography, vol. 32, no. 10, p. e4321, 2018. View at: Publisher Site | Google Scholar
  86. K. Shi, J. Zhu, D. Chen et al., “Lipidomics analysis of timosaponin BII in INS‐1 cells induced by glycolipid toxicity and its relationship with inflammation,” Chemistry & Biodiversity, vol. 17, no. 4, article e1900684, 2020. View at: Publisher Site | Google Scholar
  87. J. Hou, Y. Yun, J. Xue, B. Jeon, and S. Kim, “Doxorubicin‐induced normal breast epithelial cellular aging and its related breast cancer growth through mitochondrial autophagy and oxidative stress mitigated by ginsenoside Rh2,” Phytotherapy Research, vol. 34, no. 7, pp. 1659–1669, 2020. View at: Publisher Site | Google Scholar
  88. Y. Li, L. Wang, P. Wang et al., “Ginsenoside-Rg1 rescues stress-induced depression-like behaviors via suppression of oxidative stress and neural inflammation in rats,” Oxidative Medicine and Cellular Longevity, vol. 2020, Article ID 2325391, 15 pages, 2020. View at: Publisher Site | Google Scholar
  89. G. H. Lee, W. J. Lee, J. Hur, E. Kim, H. G. Lee, and H. G. Seo, “Ginsenoside Re mitigates 6-hydroxydopamine-induced oxidative stress through upregulation of GPX4,” Molecules, vol. 25, no. 1, p. 188, 2020. View at: Publisher Site | Google Scholar
  90. W. Li, J.-Q. Wang, Y.-D. Zhou et al., “Rare ginsenoside 20(R)-Rg3 inhibits D-galactose-induced liver and kidney injury by regulating oxidative stress-induced apoptosis,” The American Journal of Chinese Medicine, vol. 48, no. 5, pp. 1141–1157, 2020. View at: Publisher Site | Google Scholar
  91. B. Cheng, W. Gao, X. Wu et al., “Ginsenoside Rg2 ameliorates high-fat diet-induced metabolic disease through SIRT1,” Journal of Agricultural and Food Chemistry, vol. 68, no. 14, pp. 4215–4226, 2020. View at: Publisher Site | Google Scholar
  92. S.-H. Hong, H.-J. Hwang, J. W. Kim et al., “Ginsenoside compound-Mc1 attenuates oxidative stress and apoptosis in cardiomyocytes through an AMP-activated protein kinase-dependent mechanism,” Journal of Ginseng Research, vol. 44, no. 4, pp. 664–671, 2020. View at: Publisher Site | Google Scholar
  93. H.-J. Fan, Z.-B. Tan, Y.-T. Wu et al., “The role of ginsenoside Rb1, a potential natural glutathione reductase agonist, in preventing oxidative stress-induced apoptosis of H9C2 cells,” Journal of Ginseng Research, vol. 44, no. 2, pp. 258–266, 2020. View at: Publisher Site | Google Scholar
  94. J. Sun, X. Yu, H. Huangpu, and F. Yao, “Ginsenoside Rb3 protects cardiomyocytes against hypoxia/reoxygenation injury via activating the antioxidation signaling pathway of PERK/Nrf2/HMOX1,” Biomedicine and Pharmacotherapy, vol. 109, pp. 254–261, 2019. View at: Publisher Site | Google Scholar
  95. Q. Li, Y. Xiang, Y. Chen, Y. Tang, and Y. Zhang, “Ginsenoside Rg1 protects cardiomyocytes against hypoxia/reoxygenation injury via activation of Nrf2/HO-1 signaling and inhibition of JNK,” Cellular Physiology and Biochemistry, vol. 44, no. 1, pp. 21–37, 2018. View at: Publisher Site | Google Scholar
  96. Y. Gao, S. Chu, Z. Zhang, and N. Chen, “Hepataprotective effects of ginsenoside Rg1 - a review,” Journal of Ethnopharmacology, vol. 206, pp. 178–183, 2017. View at: Publisher Site | Google Scholar
  97. H. Wang, Y. M. Liu, Z. M. Qi et al., “An overview on natural polysaccharides with antioxidant properties,” Current Medicinal Chemistry, vol. 20, no. 23, pp. 2899–2913, 2013. View at: Publisher Site | Google Scholar
  98. X. Wang, J. Wang, J. Zhang, B. Zhao, J. Yao, and Y. Wang, “Structure-antioxidant relationships of sulfated galactomannan from guar gum,” International Journal of Biological Macromolecules, vol. 46, no. 1, pp. 59–66, 2010. View at: Publisher Site | Google Scholar
  99. H. Qi, Q. Zhang, T. Zhao, R. Hu, K. Zhang, and Z. Li, “In vitro antioxidant activity of acetylated and benzoylated derivatives of polysaccharide extracted from Ulva pertusa (Chlorophyta),” Bioorganic and Medicinal Chemistry Letters, vol. 16, no. 9, pp. 2441–2445, 2006. View at: Publisher Site | Google Scholar
  100. W. Pasanphan, G. R. Buettner, and S. Chirachanchai, “Chitosan gallate as a novel potential polysaccharide antioxidant: an EPR study,” Carbohydrate Research, vol. 345, no. 1, pp. 132–140, 2010. View at: Publisher Site | Google Scholar
  101. R. Jiao, Y. Liu, H. Gao, J. Xiao, and K. F. So, “The anti-oxidant and antitumor properties of plant polysaccharides,” The American Journal of Chinese Medicine, vol. 44, no. 3, pp. 463–488, 2016. View at: Publisher Site | Google Scholar
  102. A. Awad, S. R. Khalil, B. M. Hendam, R. M. Abd el-Aziz, M. M. M. Metwally, and T. S. Imam, “Protective potency of Astragalus polysaccharides against tilmicosin- induced cardiac injury via targeting oxidative stress and cell apoptosis-encoding pathways in rat,” Environmental Science and Pollution Research International, vol. 27, no. 17, pp. 20861–20875, 2020. View at: Publisher Site | Google Scholar
  103. Q. Sun, X. Wu, H. Wang et al., “Protective effects of Astragalus polysaccharides on oxidative stress in high glucose-induced or SOD2-silenced H9C2 cells based on PCR array analysis,” Diabetes, Metabolic Syndrome and Obesity, vol. 12, pp. 2209–2220, 2019. View at: Publisher Site | Google Scholar
  104. D. Li, Y. Liu, R. Xu et al., “Retracted article: Astragalus polysaccharide alleviates H2O2-triggered oxidative injury in human umbilical vein endothelial cells via promoting KLF2,” Artificial Cells, Nanomedicine, and Biotechnology, vol. 47, no. 1, pp. 2188–2195, 2019. View at: Publisher Site | Google Scholar
  105. M. R. Farag, W. M. Elhady, S. Y. A. Ahmed, H. S. A. Taha, and M. Alagawany, “Astragalus polysaccharides alleviate tilmicosin-induced toxicity in rats by inhibiting oxidative damage and modulating the expressions of HSP70, NF-kB and Nrf2/HO-1 pathway,” Research in Veterinary Science, vol. 124, pp. 137–148, 2019. View at: Publisher Site | Google Scholar
  106. L. Ou, P. Wei, M. Li, and F. Gao, “Inhibitory effect of Astragalus polysaccharide on osteoporosis in ovariectomized rats by regulating FoxO3a/Wnt signaling pathway,” Acta Cirurgica Brasileira, vol. 34, no. 5, article e201900502, 2019. View at: Publisher Site | Google Scholar
  107. X. Yan, Q.-G. Lu, L. Zeng et al., “Synergistic protection of astragalus polysaccharides and matrine against ulcerative colitis and associated lung injury in rats,” World Journal of Gastroenterology, vol. 26, no. 1, pp. 55–69, 2020. View at: Publisher Site | Google Scholar
  108. L. Liu, X.-Y. Sha, Y.-N. Wu, M. T. Chen, and J. X. Zhong, “Lycium barbarum Polysaccharides protects retinal ganglion cells against oxidative stress injury,” Neural Regeneration Research, vol. 15, no. 8, pp. 1526–1531, 2020. View at: Publisher Site | Google Scholar
  109. C. Pop, C. Berce, S. Ghibu et al., “Effects of Lycium barbarum L. polysaccharides on inflammation and oxidative stress markers in a pressure overload-induced heart failure rat model,” Molecules, vol. 25, no. 3, p. 466, 2020. View at: Publisher Site | Google Scholar
  110. F.-L. Yang, Y.-X. Wei, B.-Y. Liao et al., “Effects of Lycium barbarum polysaccharide on endoplasmic reticulum stress and oxidative stress in obese mice,” Frontiers in Pharmacology, vol. 11, p. 742, 2020. View at: Publisher Site | Google Scholar
  111. H. Amagase, B. Sun, and C. Borek, “_Lycium barbarum_ (goji) juice improves in vivo antioxidant biomarkers in serum of healthy adults,” Nutrition Research, vol. 29, no. 1, pp. 19–25, 2009. View at: Publisher Site | Google Scholar
  112. S. C. Chang, B. Y. Hsu, and B. H. Chen, “Structural characterization of polysaccharides from _Zizyphus jujuba_ and evaluation of antioxidant activity,” International Journal of Biological Macromolecules, vol. 47, no. 4, pp. 445–453, 2010. View at: Publisher Site | Google Scholar
  113. P. Ji, Y. Wei, W. Xue et al., “Characterization and antioxidative activities of polysaccharide in Chinese Angelica and its processed products,” International Journal of Biological Macromolecules, vol. 67, pp. 195–200, 2014. View at: Publisher Site | Google Scholar
  114. P. Lai and Y. Liu, “Angelica sinensispolysaccharides inhibit endothelial progenitor cell senescence through the reduction of oxidative stress and activation of the Akt/hTERT pathway,” Pharmaceutical Biology, vol. 53, no. 12, pp. 1842–1849, 2015. View at: Publisher Site | Google Scholar
  115. X. Zhang, H. Xue, P. Zhou et al., “_Angelica_ polysaccharide alleviates oxidative response damage in HaCaT cells through up-regulation of miR-126,” Experimental and Molecular Pathology, vol. 110, p. 104281, 2019. View at: Publisher Site | Google Scholar
  116. S. Y. Yoon, S. Park, and Y. Park, “The anticancer properties of Cordycepin and their underlying mechanisms,” International Journal of Molecular Sciences, vol. 19, no. 10, p. 3027, 2018. View at: Publisher Site | Google Scholar
  117. B.-J. Ke and C.-L. Lee, “Using submerged fermentation to fast increase N6-(2-hydroxyethyl)-adenosine, adenosine and polysaccharide productions of Cordyceps cicadae NTTU 868,” AMB Express, vol. 9, no. 1, p. 198, 2019. View at: Publisher Site | Google Scholar

Copyright © 2021 Bo Liang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


More related articles

 PDF Download Citation Citation
 Download other formatsMore
 Order printed copiesOrder
Views173
Downloads153
Citations

Related articles

Article of the Year Award: Outstanding research contributions of 2020, as selected by our Chief Editors. Read the winning articles.