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目的:研究蜂胶总黄酮(total flavonoids of propolis,TFP)对全脑缺血-再灌注大鼠神经元损伤的保护作用,并初步探讨其作用机制。方法:采用四血管阻断法制备大鼠全脑缺血-再灌注模型。HE染色法观察神经胶质细胞病理学变化;TUNEL法检测海马CA1区神经细胞凋亡情况;免疫组织化学法检测BCL-2、BAX蛋白的表达,并计算BCL-2/BAX比值。结果:与假手术组比较,模型组大鼠大脑皮层内神经细胞凋亡数目和BAX、BCL-2蛋白表达均显著增高,BCL-2/BAX显著降低(P<0.01);与模型组比较,TFP能显著改善缺血-再灌注大鼠脑组织病理改变,减少神经细胞凋亡数目,上调BCL-2蛋白,下调BAX蛋白,提高BCL-2/BAX比值(P<0.01),其作用具有浓度依赖性。结论:TFP对全脑缺血-再灌注大鼠脑组织损伤具有良好的保护作用,其作用机制可能与减少大脑皮层神经细胞凋亡,调节与凋亡有关的调控因子的蛋白表达有关。
Objective: To study the protective effect of total flavonoids of propolis (TFP) on neuronal damage induced by global cerebral ischemia - reperfusion in rats and its possible mechanism. Methods: A rat model of global cerebral ischemia / reperfusion was established by four-vessel occlusion. The pathological changes of glial cells were observed by HE staining. The apoptosis of neurons in CA1 area of hippocampus was detected by TUNEL method. The expressions of BCL-2 and BAX protein were detected by immunohistochemistry and the ratio of BCL-2 / BAX was calculated. Results: Compared with the sham operation group, the number of apoptotic neurons and the expressions of BAX and BCL-2 in the cerebral cortex were significantly increased and the BCL-2 / BAX was significantly decreased in the model group (P <0.01) TFP can significantly improve the pathological changes of brain tissue in ischemia-reperfusion rats, decrease the number of neuronal apoptosis, up-regulate BCL-2 protein, down-regulate BAX protein and increase BCL-2 / BAX ratio Dependency. CONCLUSION: TFP has a good protective effect on brain injury induced by global cerebral ischemia-reperfusion in rats. Its mechanism may be related to the decrease of apoptosis of neural cells in the cerebral cortex and the regulation of apoptosis-related regulatory protein.