title: [Preliminary study on hepatotoxicity induced by dioscin and its possible mechanism].
abstract: Dioscin has a wide range of biological effects and broad application prospects. However the studies concerning the toxicology and mechanism of dioscin is small. This article is to study the hepatotoxicity of dioscin and the effect of dioscin treatment on expression of aryl hydrocarbon receptor (AhR) mRNA and CYP1A mRNA and protein in HepG2 cells in vitro. Dioscin 0.5-32 µmol · L(-1) exposed to HepG2 cells for 12 h, cell viability was examined by CCK-8 assay and the release rate of lactate dehydrogenase (LDH) was to evaluate cell membrane damage. HepG2 cells morphologic changes were quantified by inverted Microscope, and the effect on production of reactive oxygen species (ROS) was detected by flow cytometry. The mRNA expression of CYP1A and AhR was evaluated by RT-RCR. The protein expression of CYP1A1 was detected by western blot. The cell viability was significantly inhibited after HepG2 cells were exposed to dioscin 0.5-32 µmol · L(-1). Compared with the control, the LDH release rate and ROS were significantly increased. The expression of CYPlA and AhR mRNA was increased. The expression of CYP1Al protein was increased after dioscin treatment, and resveratrol, an AhR antagonist, could downregulate the expression of CYP1A1. It follows that large doses dioscin has potential hepatotoxicity. The possible mechanism may be dioscin can active aryl hydrocarbon receptor (AhR) and induce the expression of CYP1A.
authors.forename: Ya-xin
authors.initials: YX
authors.lastname: Zhang
authors.forename: Yu-guang
authors.initials: YG
authors.lastname: Wang
authors.forename: Zeng-chun
authors.initials: ZC
authors.lastname: Ma
authors.forename: Xiang-lin
authors.initials: XL
authors.lastname: Tang
authors.forename: Qian-de
authors.initials: QD
authors.lastname: Liang
authors.forename: Hong-ling
authors.initials: HL
authors.lastname: Tan
authors.forename: Cheng-rong
authors.initials: CR
authors.lastname: Xiao
authors.forename: Yong-hong
authors.initials: YH
authors.lastname: Zhao
authors.forename: Yue
authors.initials: Y
authors.lastname: Gao
mesh_terms: D002470:Cell Survival / Q000187:drug effects; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology*; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics; D004144:Diosgenin / Q000031:analogs & derivatives* / Q000633:toxicity; D056945:Hep G2 Cells; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D017382:Reactive Oxygen Species / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics
chemical_list: D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D018336:Receptors, Aryl Hydrocarbon; C019357:dioscin; D007770:L-Lactate Dehydrogenase; D019363:Cytochrome P-450 CYP1A1; D004144:Diosgenin