The relationship of neuronal apoptosis and cerebral p38MAKP following liver ischemia-reperfusion iniury in rats

Objective To observe the changes of p38MAPK and apoptosis index in cerebral cortex following liver isehemia-reperfusion injury, and to evaluate the effect of p38MAPK on neuronal apoptosis. Methods A model of liver ischemia-reperfusion injury was established. The contents of p38MAPK in cortex regions and the changes of iNOS in the liver tissue were measured by immunohistochemical technique. Neuronal apoptosis was detected by TUNEL in sham operation (control group), at 30 minutes after ischemia without reperfusion (group I), reperfusion following ischemia 30 minutes (group I/R), 1 hour reperfusion following ischemia 30 minutes (group I/R 1h), 2 hour reperfusion following ischemia 30 minutes (group I/R 2h) , and 4 hours reperfusion following ischemia 30 minutes (group I/R 4h) . Results There were obvious changes of p38MAPK and neuronal apoptosis, iNOS was highly expressed in the liver tissue, especially with prolonged liver ischemia-reperfusion injury. There were positive correlations between iNOS and p38MAPK, between p38MAPK and phospho-p38MAPK, between photo-p38MAPK and apoptosis index. Eedma and infiltration of inflammatory cells, in liver tissues, as well as nacrosis, were detected by HE-staining. Conclusion Liver ischemia-reperfusion injury could cause the change of brain structure and function, and iNOS derived. As an inflammatory mediator, iNOS could lead to the increase of p38MAPK and neuronal apoptosis.