Toxicology. 2011 Sep 5 ;287(1-3):124-30. Epub 2011 Jun 16. PMID: 21704112
Ginkgolide B attenuates ethanol-induced neurotoxicity via regulating NADPH oxidases.
Ethanol has lengthy been demonstrated to set off cell apoptosis within the central nervous system. The over-production of reactive oxygen species (ROS) is taken into account as one of the vital essential mechanisms involving within the apoptosis brought on by ethanol. Ginkgolide B (GB), which was broadly used as a monomer of conventional Chinese language medication, was reported to scavenge free radicals in endothelial cells and clean muscle cells. However whether or not GB can forestall ethanol-induced neurotoxicity continues to be unknown. The purpose of this examine was to research results of GB on ethanol-induced cytotoxicity, oxidative stress and apoptosis and discover potential protecting molecular mechanism of GB. It was discovered that GB inhibited cell harm and apoptosis in a dose-dependent method in ethanol-treated PC12 cells by MTT and LDH assays. It was additionally discovered that actions of caspase-3 elevated by ethanol have been principally abrogated by GB. Additional, GB decreased the manufacturing of ROS and subsequent over-production of lipid peroxides. A big enhance of alcohol dehydrogenase (ADH) and CYP2E1 enzyme exercise was discovered within the ethanol-exposed PC12 cells as in comparison with controls. Nonetheless, GB pretreatment didn’t considerably have an effect on ethanol-induced ADH and CYP2E1 actions. Quantitative real-time PCR and Western blot evaluation demonstrated that ethanol therapy resulted in a big enhance in mRNA and protein expression of NADPH oxidases, that are foremost oxidases producing ROS in neurons. Furthermore, expression and actions of NADPH oxidases have been down-regulated by GB. These outcomes point out that ethanol-induced neurotoxicity is ameliorated by GB primarily via regulating expression and exercise of NADPH oxidases.