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 could be used as a therapeutic agent for inhibiting tumor angiogenesis.
2. Bavachinin can inhibit tube formation in human umbilical vein endothelial cells (HUVECs) as well as in vitro migration of KB cells.
3. Bavachinin decreases transcription of genes associated with angiogenesis and energy metabolism that are regulated by HIF-1, such as vascular endothelial growth factors (VEGF), Glut 1 and Hexokinase.
4. Bavachinin inhibits increases in HIF-1α activity 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.