شمس الدین احمدی

Introduction: Hepatic encephalopathy (HE) is a term that is used to describe some alterations in cerebral and cognitive functions that result from liver failures. There are different reports that HE is primarily induced by hyperammonemia and brain inflammation followed by liver failure. Mitogen-activated protein (MAP) kinases are key molecules in the signaling pathways of inflammatory and neurotransmitter receptors. It has been reported that MAP kinases are affected at transcriptional and post-transcriptional levels in hepatic encephalopathy in response to inflammation induced by hyperammonemia. The aim of the present study was to investigate expression of a main member of the MAP kinase family known as p38 MAP kinase in the hippocampus of rats with hepatic encephalopathy. Methods: Male Wistar rats weighing 300-350 g were used. Chronic liver failure was induced using a common bile duct ligation (BDL) in a group of rats as a model of HE. Sham control operation consisted of laparotomy and bile duct identification without ligation and resection. On day 28 after the surgery, the animals were decapitated, their brain were removed and the hippocampus was dissected from both hemispheres of each rat. A RT-PCR as well as western blotting methods were used for evaluating gene and protein expressions of the p38 MAP kinase in the hippocampus. The results of p38 expression between the sham control group and the group with HE was analyzed with independent sample t-test. P<0.05 was defined as statistical significant level. Results: The result of gene expression of p38 MAP kinase in the hippocampus revealed a significant decrease (P<0.01) at mRNA level in the rat model of HE group compared to sham control group. In addition, the result of western blotting method for protein expression of p38 MAP kinase in the hippocampus also showed a tendency to decrease in the group with HE compared to sham control group. Conclusion: It can be concluded that changes in p38 MAP kinase in the hippo