RESUMO
OBJECTIVE Tostudythehepatotoxicityofveratrinehydrochloride(VH)anditsmecha-nismoninductionofapoptosisinvitro.METHODS HepG2cellswereexposedtoVH0.1-0.6g·L-1 for 24 h,cell viability was examined by CCK-8 assay,and the morphologic changes in HepG2 cells were quantified.After the treatment with VH 0.1 -0.5 g·L-1 for 24 h,cell membrane injury was examined by detecting the release rate of lactate dehydrogenase (LDH).The effect on reactive oxygen species (ROS),mitochondrial membrane potential and apoptosis was detected by flow cytometry.The mRNA expression of p53,Bax,cytochrome c,caspase 9,caspase 3 was evaluated by real-time PCR. RESULTS HepG2cellviabilitywassignificantlyreducedfollowingexposuretoVH0.1-0.5g·L-1. The IC50 value was 0.4 g·L-1 .The 95%confidence limit was 0.2558-0.6965 g·L-1 .The LDH release rate,ROS and apoptosis rate of HepG2 cells were significantly increased after exposure to VH 0.1 -0.5 g·L-1 for 24 h (P<0.05,P<0.01 ),and the mitochondrial membrane potential markedly declined (P<0.05,P<0.01 ).The expression of p53,Bax,cytochrome c,caspase 9 and caspase 3 was increased(P<0.05,P<0.01).CONCLUSION VHhascytotoxicpotential.Damagetocell me mbrane and mitochondria and initiation of apoptosis-related genes of caspase 9 and caspase 3 mRNA expression may be the mechanis m of apoptosis.