1. (-)-Gallocatechin gallate can precipitate cholesterol.
2. (-)-Gallocatechin gallate decreasees osteoclastogenesis at 20 microM.
3. (-)-Gallocatechin gallate inhibits production and extracellular release of maltose binding protein and a periplasmic protein into the culture supernatant.
1. Ginkgolide C is a potent inhibitor of collagen-stimulated platelet aggregation, it may increase intracellular cAMP and cGMP production and MMP-9 activity, inhibit intracellular Ca(2+) mobilization and TXA(2) production, thereby leading to inhibition of platelet aggregation, it may be a suitable tool for a negative regulator during platelet activation.
2. Ginkgolide C has anti-adipogenic effect, it is an effective flavone for increasing lipolysis and inhibiting adipogenesis in adipocytes through the activated AMPK pathway.
3. Ginkgolide C can increase△LVP significantly,enhances the myocardial systolic and diastolic function of rats,but has no significant effect on HR while it shows inotropic activity.
1. Ginsenoside F2 has the anti-cancer activity, it induces apoptosis in breast cancer stem cells (CSCs) by activating the intrinsic apoptotic pathway and mitochondrial dysfunction, also induces the formation of acidic vesicular organelles, recruitment of GFP-LC3-II to autophagosomes, and elevation of Atg-7 levels, suggests that F2 initiates an autophagic progression in breast CSCs.
2. Ginsenoside F2 suppresses hair cell apoptosis and premature entry to catagen more effectively than finasteride, it decreases the expression of TGF-β2 and SCAP proteins, this study provides evidence those factors in the SCAP pathway could be targets for hair loss prevention drugs.
3. Ginsenoside F2 could be a new potential chemotherapeutic drug for glioblastoma multiforme (GBM) treatment by inhibiting the growth and invasion of cancer, the anticancer activity might be mediated through inhibition of proliferation judged by Ki67 and apoptosis induced by activation of caspase-3 and -8.
4. Ginsenoside F2 may reduce obesity via the inhibition of adipogenesis in the 3T3-L1 cell line.
1. 6-Gingerol has been known to possess anti-tumorigenic and pro-apoptotic activities, it stimulates apoptosis through upregulation of NAG-1 and G1 cell cycle arrest through downregulation of cyclin D1, multiple mechanisms appear to be involved in 6-gingerol action, including protein degradation as well as β-catenin, PKCε, and GSK-3β pathways.
2. 6-Gingerol and 6-shogaol may both exert anti-invasive activity against hepatoma cells through regulation of MMP-9 and TIMP-1, inhibition of the MAPK and PI3k/Akt pathways and NF-κB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis, and that 6-shogaol could further regulate urokinase-type plasminogen activity.
3. 6-Gingerol can repress quorum sensing (QS)-induced genes, specifically those related to the production of virulence factors, inducing exoprotease, rhamnolipid, and pyocyanin.
4. 6-Gingerol has antioxidant and anti-inflammatory activities, it induces genotoxicity probably by oxidative stress; lysosomal and mitochondrial damage were observed in 6-gingerol-induced toxicity.
5. 6-Gingerol has anti-adipogenic activity , can effectively suppress adipogenesis and that it exerts its role mainly through the significant down-regulation of PPARγ and C/EBPα and subsequently inhibits FAS and aP2 expression, also inhibit differentiation in 3T3-L1 cells by attenuating the Akt/GSK3β pathway.
1. Ginsenoside Rh1 has antiallergic action, may originate from its cell membrane-stabilizing and anti-inflammatory activities, and can improve the inflammation caused by allergies.
2. Ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.
3. Ginsenoside Rh1 can upregulate glucocorticoid receptor (GR) level, suggests Rh1 may improve glucocorticoid efficacy in hormone-dependent diseases, it may enhance the effect of Dex in the treatment of MRL/lpr mice through regulating CD4+ T cells activation and Th1/Th2 balance.
4. Ginsenoside Rh1 can inhibit MAPK and PI3K/Akt signaling pathways and downstream transcription factors such as NF-κB and AP-1, which play an important role in MMP gene expressions, suggests that ginsenoside Rh1 may have a therapeutic potential for malignant gliomas.
5. Ginsenoside Rh1 inhibits IFN-gamma-induced JAK/STAT and ERK signaling pathways and downstream transcription factors, and thereby iNOS gene expression, thus, the inhibition of microglial activation by ginsenoside Rh1 may provide potential therapeutic strategy for various neuroinflammatory diseases.
6. Ginsenoside Rh1 has anti-inflammatory activity, the inhibitory effects of Rh1 on monocyte function should be regarded as a promising new anti-inflammatory response with a potential therapeutic role against inflammation-dependent diseases.