| Objective: To observe the effect of ozone oxidative preconditioning on apoptosis induced by hepatic ischemia reperfusion injury in rats,to explore the protective effect of ozone on the liver and possible mechanism.Methods: Eighteen Sprague-Dawley rats(male, 6 ~ 8 weeks-old, 250 ~ 280 g) were randomly divided into three groups: ozone oxidative preconditioning group(group OP + IR, n = 6), pure ischemia reperfusion group(group IR, n = 6) and control group(group C, n = 6).Group OP + IR was received intraperitoneal injection of O3 / O2 gas mixture(ozone concentration of 50 ug/ml, 1 mg/kg/d) at the same time every day for five days;group C and group IR were received equal volume of oxygen(ml). To set up 70% of hepatic ischemia reperfusion model, group OP + IR and group IR were subjected to 45 min ischemia,then follow by 3 h perfusion,and group C was only subjected to laparotomy. The liver tissue morphology was observed, liver cell apoptosis index(AI), Bcl- 2 protein expression and Bax protein expression were determined, the Bcl- 2 / Bax ratio was computed.Results:(1) compared with group C, the liver tissue ultrastructure of group(OP+ IR) and group IR was damaged;but compared with group IR,the damage of group OP + IR was lighter.(2) compared with group C, the hepatocyte apoptosis index of group OP + IR and group IR were increased, the Bcl- 2 protein expression was decreased, Bax protein expression was increased, and the Bcl- 2 / Bax ratio was decreased(P < 0.05).(3) compared with group IR, the hepatocyte apoptosis index of group OP + IR was reduced, the Bcl- 2 protein expression was increased, Bax protein was decreased, and the Bcl- 2 / Bax ratio was increased(P < 0.05).Conclusion: ozone oxidative preconditioning may reduce apoptosis induced by hepatic ischemia reperfusion injury in rats, and it may be related to the rise of the Bcl- 2 protein ? the decrease of the Bax protein and the rise in the proportion of the Bcl-2/Bax. |
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