title: [Effect of membrane permeability transition on hepatocyte apoptosis of the microcystin-LR-induced mice].
abstract: OBJECTIVE
  From the view of membrane permeability transition (MPT) to study the mechanism of microcystin (MCs) inducing hepatocyte apoptosis in mice, and unclose the function of reactive oxygen species (ROS) in this process.
  
  
  METHODS
  Use the mice as the model animals and randomly divide them into 4 groups. Group A were injected with physiological saline peritoneal in abdomen, while group B were injected with MC-LR 50 microg/kg bw in abdomen, group C were injected with the MPT inhibitor, Cyclosporin A (CsA) 100 mg/kg bw, in abdomen, and group D were injected with CsA 100 mg/kg bw in abdomen, and then after 1 hour, with MC-LR 50 microg/kg bw. Separate the mice serum, measure AST and ALT concentrations. Separate the mice livers and then perform the mice liver DNA segment detection, mitochondrion membrane potential level measurement, ROS level measurement and western blotting measurement at the expression level of Bcl-2.
  
  
  RESULTS
  In the group treated with 50 microg/kg bw MC-LR, in the serum, the AST and ALT levels rised. In the liver cells, there was significant DNA ladder, the the expression of Bcl-2 at the level of protein increased, mitochondrion membrane potential level of liver tissue decreased, and the ROS level in the tissue increased. In the group treated with 100 mg/kg bw CsA, every index of the mice has no significant change. While with the pre-treatment of 100 mg/kg bw CsA, and then with 50 microg/kg bw MC-LR in abdomen, the DNA ladder in the liver tissue can be removed, and the serum AST and ALT concentrations, the expression of liver Bcl-2 protein, the mitochondrion membrane potential level and ROS level were conversed to the levels of the control group.
  
  
  CONCLUSIONS
  In vivo the inhibition of transition channel of mitochondrion membrane can inhibit the hepatocyte apoptosis induced by MC-LR.
authors: National Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210093, China.
authors: Jing
authors: J
authors: Liu
authors: Yinna
authors: Y
authors: Wei
authors: Pingping
authors: P
authors: Shen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D016572:Cyclosporine / Q000494:pharmacology; D022781:Hepatocytes / Q000166:cytology*; D008297:Male; D008387:Marine Toxins; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D008813:Mice, Inbred ICR; D052998:Microcystins / Q000633:toxicity*; D033681:Mitochondrial Membrane Transport Proteins / Q000187:drug effects* / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D008387:Marine Toxins; D052998:Microcystins; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species; D016572:Cyclosporine; C057862:cyanoginosin LR