| Objective:Chronic cerebral ischemia models were established by permanent bilateral common carotid artery occlusion(BCCAO).Intervention with Ethyl Pyruvate(EP)was performed to observe the pathological changes of neurons and the expression of apoptosis-related proteins Bcl-2 and Bax in the frontal cortex and hippocampus of rats.To investigate the effect of Ethyl Pyruvate(EP)on the expression of apoptosis-related proteins Bcl-2 and Bax in rats with chronic cerebral ischemia and neuroprotective effects.Methods:There were 24 healthy male Sprague-Dawley rats(200-250 g),that were averagely divided into 4 groups: sham operation group(6 rats),model group(6 rats),EP low-dose group(6 rats),and EP high-dose group 6 rats).In the sham operation group,only the bilateral common carotid arteries were isolated and not ligated.In the other three groups,the rat model of chronic cerebral ischemia was prepared by ligation of bilateral common carotid arteries.The low dose group was intraperitoneally injected with EP 25 mg/kg/d,and the high dose group was intraperitoneally injected with EP 50 mg/kg/d.Each group was perfused with a decapitated brain within 4 weeks.The pathological changes of neurons in frontal cortex and hippocampus were observed by HE staining.The damage of neurons in frontal cortex and hippocampus was observed by Nissl staining.The rats in each group were detected by immunohistochemistry.Expression of Bcl-2 and Bax proteins in frontal cortex and hippocampus.Results:1.Compared with the sham-operated group,neurons in the frontal cortex and hippocampus of the model group showed obvious apoptotic phenomena,especially in the hippocampus.2.Compared with the model group,neuronal apoptosis in the frontal cortex and hippocampus of EP treatment group was significantly reduced,and that in the high-dose group was more obvious than that in the low-dose group.3.Compared with the sham-operated group,the expression of Bcl-2 in frontal cortex and hippocampus of the model group was significantly decreased(P < 0.05),and the expression of Bax was significantly increased(P < 0.05).4.Compared with the model group,the expression of Bcl-2 and Bax in frontal cortex and hippocampus increased significantly(P < 0.05)and decreased significantly(P < 0.05)in the EP treatment group,especially in the EP high dose group.Conclusion:Ethyl pyruvate can inhibit hippocampal neuronal apoptosis in chronic cerebral ischemia rats,and its mechanism may be related to EP involved in the regulation of apoptosis-related protein expression. |
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