1. Meliasenin B displays dose-dependent toxicity on HepG2 cells, suggests that it may cause hepatotoxicity.
1. Palmitic acid induces down-regulation of APOM expression, is mediated via the PPARβ/δ pathway.
2. Palmitic acid induces anxiety-like behavior in mice while increasing amygdala-based serotonin metabolism.
3. Palmitic acid induces degeneration of myofibrils and modulate apoptosis in rat adult cardiomyocytes.
4. Many of the deleterious effects of high-fat diets, specifically those enriched with palmitic acid, are CNS mediated via PKC-theta activation, resulting in reduced insulin activity.
5. Palmitic acid induces production of proinflammatory cytokine interleukin-8 from hepatocytes.
6. Palmitic acid induces apoptosis in the human leukemic cell line MOLT-4 at 50 micrograms/ml, it also shows in vivo antitumor activity in mice, suggesting that palmitic acid may be a lead compound of anticancer drugs.
1. Dictamnine and gamma-fagarine have mutagenic activities, they have specific activities (His+/microgram) of about 50-70 revertant colonies in strain TA100, while in strain TA98 there were about 30-50 revertant colonies.
2. Dictamnine has good antifungal activity alone and in combination with fluconazole against Candida albicans.
3. Dictamnine at higher concentrations(≥100uM) has potential hepatotoxicity, the cell membrane damage and mitochondrial membrane damage may be involved in the dictamnine-induced hepatotoxity mechanism.
4. Dictamnine has photoinduced genotoxicity.
5. Dictamnine shows anti-inflammatory effect.
6. Dictamnine shows anticholinesterase activityt.
1. Deoxycholic acid is a strong promoter of hepatocarcinogenesis with possible complete carcinogenicity in the liver and promotion potential for tumor development in the small intestine.
2. Loss of deoxycholic acid-induced EGFR/Ras/MAPK pathway function potentiates deoxycholic acid-stimulated FAS-induced hepatocyte cell death via a reduction in the expression of c-FLIP isoforms.
3. Hyaluronic acid-Deoxycholic acid conjugates are a good candidate for drug delivery and could potentiate therapeutic formulations for doxorubicin-mediated cancer therapy.
1. Bavachinin(BVC) has antiinflammatory, antipyretic and analgesic properties.
2. Bavachinin has potent anti-angiogenic activity in vitro and in vivo; it inhibits increases in HIF-1αactivity in human KB carcinoma (HeLa cell derivative) and human HOS osteosarcoma cells under hypoxia in a concentration-dependent manner, probably by enhancing the interaction between von Hippel-Lindau (VHL) and HIF-1α.
3. Bavachinin has the potential as a potent anti-asthma drug.
4. Bavachinin has been reported to demonstrate peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist activity, (S)- and (R)-bavachinin demonstrate similar PPAR-γ agonist activities.
5. Bavachinin exhibits glucose-lowering properties without inducing weight gain and hepatotoxicity, BVC synergised with thiazolidinediones, which are synthetic PPAR-γ agonists, and fibrates, which are PPAR-α agonists, to induce PPAR transcriptional activity, as well as to lower glucose and triacylglycerol levels in db/db mice.