Effects of Ozone Oxidative Preconditioning on Apoptosis Induced by Hepatic Ischemia Reperfusion Injury in Rats

OBJECTIVE To observe the effect of ozone oxidative preconditioning on apoptosis induced by hepatic ischemia reperfusion injury in rats, and explore the protective effect of ozone on the liver and possible mechanism. METHODS Eighteen SD rats (♂, 6-8 weeks old, 250-280 g) were randomly divided into three groups: ozone oxidative preconditioning group(OP+IR group), pure ischemia reperfusion group (IR group) and sham operation group (S group), six rats in each group. OP+IR group were received intraperitoneal injection of O₃/O₂ gas mixture (O₃ concentration of 50 μg·mL^-1, 1 mg·kg^-1·d^-1) at the same time every day for 5 d; S group and IR group were received equal volume of O₂. To set up 70% of hepatic ischemia reperfusion model, OP+IR group and IR group were subjected to 45 min ischemia, then follow by 3 h perfusion, and S group 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 Compared with S group, the liver tissue ultrastructure of OP+IR group and IR group was damaged; but compared with IR group, the damage of OP+IR group was lighter. Compared with S group, the hepatocyte apoptosis index of OP+IR group and IR group 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). Compared with IR group, the hepatocyte apoptosis index of OP+IR group 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 O₃ 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.