Effect of Puerarin on the expression of c-fos protein and Bcl-2 protein in cardiac tissue following liver ischemia-reperfusion injury in rats

Objective:To observe the changes of c-fos protein and Bcl-2 protein in brain tis sue following liver ischemia-reperfusion injury and evaluate the contribution of two factors to brain cell apoptosis,to explore the effects of puerarin on the injury mechanisms.Methods:A model of liver ischemia-reperfusion injury was established by imitation.56 healthy rats were randomly divided into 7 groups as following(n=8):the control group(the group of sham operation),simply ischemia 30 min without reperfusion(I group),reperfusion following ischemia 30 min(I/R group),1 hour reperfusion following ischemia 30 min(I/R 1 h group),2 hour reperfusion following ischemia 30 min(I/R 2 h group),4 hour reperfusion following ishcemia 30 min(I/R 4 h group),and puerarin pretreat ment group(PUE+I/R 4 h).Liver and brain tissue were observed by HE staining.The expressions of c-fos protein and Bcl-2 protein in brain tissue were examined individually by immunohistochemical technique in each group.The changes of brain cell apoptosis were measured by TUNEL labelling technique.Results:Liver ischemia/reperfusion induced the remarkable brain cell injury.The con tents of c-fos protein and Bcl-2 protein increased in I group and reached to the peak in I/R 4 h group(P0.01).The index of apoptosis in brain cells showed increasing during different phase of liver is chemia-reperfusion injury(P0.01).The injury of brain cell in PUE+ I/R 4 h group was less than that of I/R 2 h group and I/R 4 h group(P0.01).Conclusion:The injury of brain tissue and brain cell apoptosis might be induced following the process of liver ischemia/reperfusion injury.c-fos showed increasing and might be involved in the mechanism of liver cell apoptosis.Bcl-2 could play the role in anti-liver cell apoptosis during the period of liver ischemia-reperfusion.Puerarin pretreatment had an protect effect on brain injury by restraining expressions of c-fos protein and increasing contents of Bcl-2 protein at hepatic isehemia reperfusion.