|
| Activity | Result of mechanism | Mechanism | Authors |
|
| Prevention of anaphylaxis | (i) Inhibition of mast cell degranulation
(ii) Reduction the activation of the PLCγ-PKC-IP3 signaling pathway | (i) Inhibition of Ca2+ flow
(ii) Inhibition of MCP-1, IL-8, β-hexosaminidase, HA, and TNF-α release
(iii) Inhibition of phosphorylation of PLCγ1, IP3R, PKC, Akt, P38, and Erk1/2 | [57] |
|
| Alleviation of polycystic ovary syndrome | (i) Reduction of cysts
(ii) Regulation of the hormonal balance
(iii) Restoration of the ovulation cycle | (i) Reversion of the expression of genes Star, Hsd3b1, Cyp11a1 (increase), and Cyp19a1 (reduction)
(ii) Increase in antioxidant enzyme activities (SOD, GSH-Px, and CAT)
(iii) Regulation of the level of T, E2, FSH, P4, and AMH and the ratio of LH/FSH in serum
(iv) Reduction of MDA level and enhanced GSH content and GSH/GSSG ratio | [46] |
|
| Antitumor effects | (i) Induction of cisplatin sensitivity by JNK and P38 MAPK signaling pathway | (i) Increase in P-JNK and P-38 levels | [45] |
| (i) Inhibition of cancer cell proliferation | (i) Inhibition of Skov3 cell proliferation
(ii) Reduction of WSB1 expression
(iii) Inhibition of Erk1/2 expression and Erk phosphorylation | [90] |
(i) Inhibition of cancer cell proliferation
(ii) Induction of cancer cell apoptosis | (i) Inhibition of the MCF-7 cell cycle at the S phase
(ii) Reduction of CDK2, cyclin D1, and cyclin E levels
(iii) Reduction of p-PI3K, PI3K, AKT, and p-AKT levels | [51] |
| (i) Inhibition of tumor angiogenesis | (i) Inhibition of p38 MAPK phosphorylation
(ii) Reduction of MMP-2 and MMP-9 levels
(iii) Reduction of COX-2 expression by p38MAPK/ATF-2 signaling pathway (by inhibition of p38MAPK phosphorylation)
(iv) Increase of the caspase-3 cleavage in tumor cells | [91] |
| (i) Induction of autophagy in cancer cells by regulating Beclin 1 and ERK expression | (i) Increase in Beclin 1 and LC3-II expression in tumor cells
(ii) Reduction of phosphorylated ERK1/2 expression and p62 level in tumor cells | [94] |
| (i) Induction of apoptosis of tumor cells by regulating the NF-κB signaling pathway (inhibition of the tumor growth) | (i) Inhibition of the expression of ICAM1, MMP9, TNF-α, and VCAM1
(ii) Increase in the expression of p-IκBα and pP65 | [92] |
|
| Alleviation of damage and brain injuries | (i) Inhibition of the activation of the pyroptotic pathway and apoptosis of injured nerves
(ii) Activation of damage mitigating factor | (i) Reduction of cytokine expression (NLRP3, ASC, caspase-1, GSDMD, IL-1β, IL-18, LDH, NF-κB, and p-p56)
(ii) Changes in activation of the NF-κB signaling pathway | [63] |
(i) Reduction of the apoptosis and autophagy of neural stem cells by modulation of the p38/MAPK/MK2/Hsp27-78 signaling pathway
(ii) Stimulation of the cell proliferation | (i) Reduction of p38 and Hsp27-78 phosphorylation and MK-2, Bax, cleaved caspase-3, LC3-II, and mTOR phosphorylation expression
(ii) Increase in Bcl-2 and p62 expression | [65] |
(i) Inhibition of dopamine synthesis
(ii) Promotion α-syn clearance by regulating autophagy | (i) Increase in the formation of autophagosomes
(ii) Increase of TH, p-JNK1/JNK1, Beclin 1, Atg7, Atg12-5, and p-Bcl-2/Bcl-2 expression and the LC3-II/LC3-I ratio
(iii) Reduction of α-syn expression | [66] |
|
| Alleviation of diabetes complications | (i) Inhibition of JNK/c-Jun signaling pathway
(ii) Alleviation of oxidative damage | (i) Inhibition of p-JNK and p-c-Jun activation
(ii) Reduction of phosphorylation of JNK and c-Jun
(iii) Reduction of cleaved parp and cleaved caspase-3 levels | [44] |
(i) Promotion of PI3K and Akt activation
(ii) Inhibition of the apoptosis of pancreatic β-cells | (i) Increase of PI3K, AKT, and p-AKT expressions
(ii) Increase in contents of hepatic glycogen and glycogen synthase in the liver | [59] |
(i) Reduction of renal fibrosis
(ii) Regulation of the TLR4/NF-κB(p65) pathway and miRNA-140-5p level | (i) Increase of miRNA-140-5p mRNA, BG, 24 h UP, TC, TG, T-AOC, MDA, IL-6, TNF-α, TLR4, NF-κB(p65), NLRP3, Notch2, and Col-IV | [60] |
|
| Protection of the digestive system | (i) Protection of the liver and other organs against aging | (i) Increase of CAT, GSH-Px, MDA, and SOD activities
(ii) Reduction of the mRNA, protein level of cyclin-dependent kinase inhibitor p16 and phosphorylation of pRb
(iii) Increase in CDK4/6 protein expression | [86] |
| (i) Protection of the liver against damage | (i) Reduction of ALT, ALP, AST, and total bilirubin levels | [87] |
|
| Protection and treatment of cardiovascular diseases | (i) Change in platelet activation pathway | (i) Regulation of core genes: PRKACA, PIK3R1, MAPK1, PPP1CC, PIK3CA, and SYK | [76] |
| (i) Inhibition of activation of the JAK2/STAT1 pathway | (i) Inhibition of caspase-3 activity (reduction of H/R-induced apoptosis)
(ii) Reduction of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 1 (STAT1) activity
(iii) Reduction of releases of cTnI, IL-6, and LdH
(iv) Change of expression levels of Bcl-2-associated X protein, Bcl-2, cleaved caspase-3, Fas ligand, and tumor necrosis factor receptor superfamily member 6 (Fas) | [47] |
| (i) Effect on vasodilation | (i) Inhibition of the PKA and NO production
(ii) Activation of p-eNOS expression
(iii) Change of the influx of Ca2+ (TRPV4-dependent) | [81] |
|
| Protection of skeletal system | (i) Regulation of pVHL/HIF-1α/VEGF pathway
(ii) Increase in angiogenesis and bone cell differentiation
(iii) Inhibition of HIF-1α expression | (i) Increase of ALP, Ang-2 (Angiopoietin-2), HIF-1α (hypoxia inducible factor-1α), OPN-1 (osteopontin-1), Runx2 (runt-related transcription factor 2), and VEGF (vascular endothelial growth factor) levels
(ii) Inhibition of SY-induced proliferation, migration, and angiogenesis | [69] |
(i) Increase in osteoblast differentiation
(ii) Inhibition of osteoblast apoptosis | (i) Inhibition of caspase-3 activity (change in caspase-3-dependent signaling pathway) | [70] |
|
| Protection of the respiratory system | (i) Inhibition of the platelet activating factor in the airway epithelium
(ii) Reduction of inflammation | (i) Changes in the expression of interleukin- (IL-) 1β and IL-6, inflammatory signaling pathways, monolayer permeability of HSAECs, and tumor necrosis factor alpha
(ii) Reduction of inflammatory factor expression and nuclear factor-κB activation
(iii) Inhibition of activator protein-1, protein kinase C, and mitogen-activated protein kinase expression | [74] |
|
| Reduction of overweight and obesity | (i) Change in the composition of intestinal microflora
(ii) Restoration of glucose homeostasis
(iii) Alleviate insulin resistance | (i) Changes in pathways of sphingolipid and glycerophospholipid metabolisms
(ii) Increase of L-carnitine, lysophosphatidylcholine, and sphingomyelin levels
(iii) Reduction of phosphatidylcholines | [67] |
| (i) Increase in the synthesis of antioxidant enzymes in adipose tissue and in the liver | (i) Increase of expression of antioxidant enzymes and Nrf2 in adipocytes, liver tissue, and HepG2 cells
(ii) Regulation of glucose metabolism and liver function | [50] |
|
