Bilobetin

Bilobetin, an active component of Ginkgo biloba, can reduce blood lipids and improve the effects of insulin. Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in β-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPARα accompanied by elevated cAMP level and PKA activity^[1]. In Vitro:Bilobetin (0-40 μM, 24/48/72 h) inhibits the cell proliferation in Huh7 and HepG2 cells^[4].
Bilobetin (0-20 μM, 24 and 48 h) induces apoptosis and increases sub G1 population in Huh7 and HepG2 cells^[4].
Bilobetin (0-20 μM, 24 h) induces accumulation of ROS and DNA damage in Huh7 and HepG2 cells^[4].
Bilobetin (1-2 μM, 1 days) inhibits the phosphorylation of AKT in sebocytes^[5]. In Vivo:Bilobetin (i.p., 12 mg/kg/day, 4 or 14 days) ameliorates hyperlipidaemia, lipotoxicity and insulin resistance by PKA-mediated phosphorylation of PPARα in rats fed a high-fat diet^[1].
Bilobetin (i.p., 50 mg/kg, for 7 days) induces kidney injury in rats, and promotes the trafficking of AQP-2 onto the plasma membrane in rats^[2].
Bilobetin (6 and 12 mg/kg, i.p., daily for ten days.) shows protective effects against Cisplatin (HY-17394) (7 mg/kg, i.p., a single dose on the third day)-induced testicular toxicity in rats^[3].