Mediators of Inflammation / 2014 / Article / Tab 1

Review Article

Integrating Traditional Medicine into Modern Inflammatory Diseases Care: Multitargeting by Rhus verniciflua Stokes

Table 1

Biological activities of Rhus verniciflua Stokes as shown in in vitro studies.

Exhibited activity against H. pylori [6].
(i) Exhibited 70% cell death in HeLa and CT-26 tumor cell lines at a minimum concentration of 2.48  M [7].
(ii) Increased DNA fragmentation on the human B and T lymphoma cell lines, BJAB and Jurkat [8].
(iii) Exhibited apoptosis via caspase-8/PARP cleavage pathway in human osteosarcoma cells [9].
(iv) Exhibited apoptosis induction on SV40-mediated transformed embryonic hepatic cells [10].
(v) Induced apoptosis through an intrinsic pathway in gastric cancer cell lines [11].
(vi) Exhibited caspase-independent death of human osteosarcoma cells via p53-mediated mitochondrial stress and nuclear translocation of AIF and endonuclease G [12].
(vii) Enhanced mitochondrial mediated apoptosis by inhibition of the PI3K-Akt/PKB survival pathway in gastric cancer cell lines [13].
(viii) Exhibited potential organ-specific anticancer activity [14].
Antigrowth activity
(i) Inhibited cell proliferation in cultured HeLa and CT-26 tumor cells [7].
(ii) Inhibited the growth of human B, BJAB, and T lymphoma cell lines, Jurkat [8, 15].
(iii) Exhibited sensitive growth inhibition in human osteosarcoma cells [9].
(iv) Exhibited a selective growth inhibition on SV40-mediated transformed embryonic hepatic cells [10].
(v) Exhibited a synergistic inhibitory effect on cell growth in gastric cancer cells at 50  g/mL [11].
(vi) Inhibited the clonogenic growth of small numbers of UACC-812 breast cancer cells cocultured with fibroblasts in vitro [16].
(vii) Suppressed mouse macrophage cell proliferation [17].
(i) Suppressed proinflammatory mediators NO, PGE2, and TNF-α via inhibition of NF- B and JNK pathway in LPS-induced RAW 264.7 macrophages [18].
(ii) Inhibited ROS production and PKC- translocation, downregulated the expression of NF- B and AP-1, and inhibited the levels of iNOS and COX-2 expression [19].
(iii) Inhibited the expressions of TNF- , IL-6, and IL-8 on human mast cells with treatment with PMA and A23187 [20].
(iv) Inhibited LPS-induced NO, PGE2, TNF- , and IL-1 production via the induction of HO-1 expression in murine macrophages [21].
(v) Suppressed NOS via the ERK and Akt signaling pathways [22].
(vi) Suppressed iNOS and COX2 mRNA expression induced by LPS and decreased intracellular ROS levels induced by LPS [17].
(vii) Inhibited inflammation-related cytokines and angiogenic factor in rheumatoid arthritic fibroblast-like synovial cells [23].
(viii) Suppressed 2,4-DNFB-induced allergic contact dermatitis [24].
(i) Exhibited the inhibition of hydroxyl radical-mediated degradation by iron ion chelation [25].
(ii) Exhibited the inhibition of linoleic acid oxidation, protected human LDL from oxidative modification, and protected against plasmid DNA strand breakage induced by peroxyl free radicals [26].
(iii) Exhibited against hydroxyl and peroxyl radicals in in vitro assays [7].
(iv) Inhibited activities of NF- B and AP-1 induced by G/GO [27].
(v) Reduced intracellular ROS formation caused by H2O2, reduced TBARS formation, and attenuated catalase depletion at concentration of 100  /mL [28].
(vi) Prevented cisplatin-induced ROS release against MDCK-I cells [29].
(vii) Protected human keratinocytes against oxidative stress caused by H2O2 [30].
Exhibited antiviral activity against fish pathogenic IHNV and VHSV [31].
(i) Protected the murine hippocampal HT22 cells against glutamate-induced neurotoxicity [32].
(ii) Protected dopaminergic neuronal cells in a rotenone model of PD [33].
(iii) Protected against 6-OHDA-induced neuronal cell death of PD [34].
(iv) Protected against rotenone-induced toxicity by preventing the downregulation of BDNF and GDNF in human dopaminergic cells, SH-SY5Y [35, 36].
Other activities
(i) Inhibited platelet aggregation via inhibition of receptor expression on platelet membranes, including glycoprotein IIb/IIIa (CD41), GPIIb/IIIa-like expression (PAC-1), and P-selectin (CD62), and intracellular calcium mobilization responses and decreased platelet activation were observed for the isomaltol- and pentagalloyl glucose-treated platelets [37].
(ii) Exhibited anti-AKR1B10 activity at 1  M with an IC50 value of 1.47  M [38].
(iii) Suppressed IL-4 and -10 in BPA-stimulated primary cultured mouse lymphocytes [39].

AIF: apoptosis-inducing factor; AKR1B10: Aldo-keto reductase family 1 B10; AP-1: activator protein-1; BDNF: brain-derived neurotrophic factor; BPA: bisphenol A; COX-2: cyclooxygenase-2; DNA: deoxyribonucleic acid; 2,4-DNFB: 2,4-dinitrofluorobenzene; GDNF: glial cell line-derived neurotrophic factor; G/GO: glucose/glucose oxidase; HO: heme oxygenase; H. pylori: Helicobacter pylori; IC50: the half maximal inhibitory concentration; IHNV: infectious hematopoietic necrosis virus; IL: interleukin; iNOS: inducible nitric oxide synthase; JNK: c-Jun NH(2)-terminal kinase; LDL: low-density lipoprotein; LPS: lipopolysaccharide; NF-κB: nuclear factor kappa B; NO: nitric oxide; NOS: nitric oxide synthase; OHDA: hydroxydopamine; PARP: poly (ADP-ribose) polymerase; PD: Parkinson's disease; PGE2: prostaglandin E2; PI3K: Phosphatidylinositide 3-kinases; PKB: protein kinase B; PKC: protein kinase C; PMA: phorbol 12-myristate 13-acetate; ROS: reactive oxygen species; SV40: Simian virus 40; TBARS: thiobarbituric acid reactive substance; TNF: tumor necrosis factor; VHSV: viral hemorrhagic septicemia virus.

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