论文部分内容阅读
目的考察5,6-二羟乙基黄芩苷对脑缺血再灌注所致神经元损伤的保护作用,并探讨其可能的作用机制。方法采用大鼠双侧颈总动脉阻断合并降压法导致全脑缺血再灌注损伤模型,用HE染色法观察大鼠海马CA1区神经元形态变化;TUNEL法测定海马CA1区神经细胞凋亡的数量;免疫组织化学法检测大鼠海马CA1区Bcl-2、Bax与Caspase-3蛋白的表达。结果 5,6-二羟乙基黄芩苷各给药组能够剂量依赖性地减少TUNEL阳性凋亡细胞的数量,下调促凋亡蛋白Bax及Caspase-3的表达,上调抑凋亡蛋白Bcl-2的表达,并不同程度地改善了大鼠海马CA1区神经元的病理改变。结论 5,6-二羟乙基黄芩苷对脑缺血再灌注损伤具有显著的保护作用,其作用机制可能与抗神经元凋亡有关。
Objective To investigate the protective effect of 5,6-dihydroxyethyl baicalin on neuronal injury induced by cerebral ischemia-reperfusion and to explore its possible mechanism. Methods The bilateral common carotid artery occlusion and antihypertensive treatment led to the model of global cerebral ischemia-reperfusion injury. The morphological changes of hippocampal CA1 neurons were observed by HE staining. The apoptosis of hippocampal CA1 neurons was detected by TUNEL method . The expression of Bcl-2, Bax and Caspase-3 protein in hippocampal CA1 region of rats were detected by immunohistochemistry. Results The results showed that 5,6-dihydroxyethyl baicalin could decrease the number of apoptotic TUNEL-positive cells, decrease the expression of pro-apoptotic proteins Bax and Caspase-3, up-regulate the expression of Bcl-2 , And to a certain extent, improved the pathological changes of neurons in CA1 area of rat hippocampus. Conclusion 5, 6-dihydroxyethyl baicalin has a significant protective effect on cerebral ischemia-reperfusion injury, and its mechanism may be related to anti-neuronal apoptosis.