The Influence Of Estradiol On Expression Of Nitric Oxide Synthase And Cell Apoptosis During The Rat Hepatic Ischemia-Reperfusion Injury

Objective To investigate the influence of estrogen on the expression of inducible nitric oxide synthase(iNOS) and endothelial nitric oxide synthase(eNOS), and cell apoptosis of hepatocytes during the rat hepatic ischemia-reperfusion injury (HIRI), and to go a step further to investigate its mechanism in order to provide experimental basis and theoretical guidance in the therapy of hepatic ischemia-reperfusion injury clinically. Methods The rats were divided into four groups as group A: male group, group B: OVX group, group C: female control group (false operative group), group D: OVX+E2 group. The rats of HIRI were established in vivo. The changes in levels of estradiol in blood serum of the liver were observed 6, 12, 24h after hepatic ischemia-reperfusion respectively. Meanwhile the expression of NOS and apoptosis of hepatocytes were detected by immunohistochemistry method. Results â‘ The levels of estradiol in blood serum: The estradiol levels of group A and B were both low at different time, and there was no significant difference between them (P>0.05). The estradiol level of group C increased and that of group D group was the highest. There was significant difference among all the groups except group A and B. â‘¡The expression of NOS in the liver: There was a little expression of iNOS in hepatocytes and Kupffer's cell (KC) of each group at the 6h reperfusion point, and there was expression of eNOS in hepatic sinusoidal endothelial cell(SEC). The expression of iNOS was obviously higher but that of eNOS was obviously lower at the 12 and 24h reperfusion point than that at the 6h reperfusion point. There was significant difference among groups with the exception of the comparision between group A and B, comparision between group C and D.(P<0.05). â‘¢The levels of hepatocytes apoptosis: There were a little hepatocytes apoptosis at the 6h reperfusion point, and there was no significant difference among groups (P>0.05). The apoptosis of hepatocytes were significantly higher at the 12 and 24h reperfusion point than that at the 6h reperfusion point. The positive expression cells of NOS shared the same distributing time and area with the apoptosis cells. The apoptosis of hepatocytes in group D and group C were significantly lower than those in group B and group A of the same time (P<0.05). The expressions of eNOS in group D and group C were significantly higher than those in group B and group A (P<0.05). The expressions of iNOS in group D and group C were significantly lower than those in group B and group A (P<0.05). Conclusion Estrogen promotes the expression of eNOS, inhibits the expression of iNOS, decreases hepatocytes apoptosis after hepatic ischemia-reperfusion injury in rats. This may be one of the mechanisms in which estrogen exerts its liver-protection in hepatic ischemia-reperfusion injury in rats.