5,6-二羟乙基黄芩苷对大鼠急性脑缺血再灌注所致海马神经细胞凋亡的保护作用

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。

Protective effects of 5,6-dihydroxyethyl bai-calin against cerebral ischemia reperfusion injury (CIR) in rats

Objective To investigate the protective effects of 5,6-dihydroxyethyl baicalin against cerebral ischemia reperfusion injury (CIR) in animal models and its possible pharmacological mechanism. Methods CIR rats model of bilateral common carotid arteries occlusion (BCCAO) repeatedly with depressurization was established. The morphology of cerebral hippocampus was determined by HE staining. The number of apoptotic cells in CA1 hippocampus was examined by TUNEL assay. Immunohistochemistry method was used to measure Bcl-2, Bax and Caspase-3 protein expression level in hippocampus of rats. Results Compared with model rats, administration of 5,6-dihydroxyethyl baicalin decreased the number of apoptotic cells in hippocampus CA1 region. 5,6-dihydroxyethyl baicalin also upregulated the expression of Bcl-2, downregulated the expression of Bax and Caspase-3, and improved the pathological changes in hippocampus of model rats. Conclusions 5,6-dihydroxyethyl baicalin has protective effects against CIR. The mechanism may be associated with the inhibition of neuronal apoptosis.