شمس الدین احمدی

Introduction: Previous reports have proposed a critical role for calcium-calmodulin dependent protein kinase IIα (CaMKIIα) in signaling cascades involved in pathogenesis of hepatic encephalopathy in the brain. The aim of the present study was to examine changes in gene expression of CaMKIIα at mRNA level in brain of a rat model with hepatic encephalopathy. Methods: Male Wistar rats weighing 280-320 g were used. For induction of hepatic encephalopathy the common bile duct was transected but sham operation consisted of laparotomy and bile duct identification without ligation and resection. On day 28 of the surgery, the animals were decapitated and brain areas including the prefrontal cortex, the cerebellar cortex and the hippocampus were bilaterally dissected from cerebral hemispheres. A semi-quantitative RT-PCR method was used for evaluating gene expression of the CaMKIIα in the mentioned brain areas. The results of gene expression between sham control group and the group with hepatic encephalopathy were analyzed with independent t-test. P<0.05 was considered as statistical significant level. Results: The results revealed that the CaMKIIα gene expression in rats with hepatic encephalopathy compared to sham control group was significantly increased in the cerebellar cortex but decreased in the hippocampus. However, the results showed that the CaMKIIα gene expression remained without significant change in the prefrontal cortex. Conclusion: The results of the CaMKIIα gene expression propose that the hepatic encephalopathy may result, at least in part, from changes in the CaMKIIα gene expression in the cerebellar cortex and hippocampus. According to the results, it can be also concluded that the CaMKIIα gene expression in different brain areas is site-specific.