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目的:探讨脑缺血再灌注后乙酰葛根素的脑保护作用及其机制。方法:线栓法制作脑缺血再灌注模型,为假手术组、脑缺血再灌注组、胞磷胆碱组(0.6 mg·kg-1)、乙酰葛根素低、中、高剂量(10,50,250 mg·kg-1)i,g 10 d干预组。采用TUNEL法检测脑组织细胞凋亡情况,采用免疫组化方法观测各组大鼠脑内PI3-K(磷脂酰肌醇-3-激酶)和Akt(丝氨酸/苏氨酸蛋白激酶)的表达情况并进行神经功能缺损评分。结果:乙酰葛根素3个剂量组神经功能评分比模型组显著改善(P<0.01),凋亡细胞数也显著下降(P<0.01),脑组织PI3-K和Akt表达显著升高(P<0.01),且呈量效关系,高剂量组较胞磷胆碱组疗效显著(P<0.05)。结论:激活PI3-K/Akt信号通路可能是乙酰葛根素减少神经细胞凋亡、起到神经保护作用的机制之一。
Objective: To investigate the protective effects of acetyl puerarin on cerebral ischemia-reperfusion and its mechanism. Methods: The model of cerebral ischemia-reperfusion was established by the method of thread occlusion. The rats in sham operation group, cerebral ischemia / reperfusion group, citicoline group (0.6 mg · kg -1), low, medium and high dose of acetylpuerarin , 50, 250 mg · kg-1) i, g 10 d intervention group. The apoptosis of brain tissue was detected by TUNEL method. The expression of PI3-K (phosphatidylinositol-3-kinase) and Akt (serine / threonine protein kinase) in the brain of each group was observed by immunohistochemistry And neurological deficit score. Results: The neurological score of acetylpuerarin in 3 doses group was significantly improved (P <0.01), the number of apoptotic cells was also significantly decreased (P <0.01), the expression of PI3-K and Akt in brain tissue was significantly increased (P < 0.01), and the dose-effect relationship, high-dose group compared with citicoline group curative effect (P <0.05). Conclusion: Activation of PI3-K / Akt signaling pathway may be one of the mechanisms by which acetyl puerarin reduces neuronal apoptosis and plays a neuroprotective role.