【摘要】 目的:探讨红景天苷对缺血再灌注大鼠脑组织损伤的保护作用及其机制。方法:用线栓法制备SD大鼠大脑中动脉栓塞模型(middle cerebralartery occlusion,MCAO)。在缺血和再灌注即刻分别给予红景天苷(2.5、5、10mg/kg)进行保护。脑缺血1.5h再灌注24h后用Zea-Longa标准进行神经功能评分;TTC染色法测定大鼠脑梗死面积;比色法测定大鼠脑组织内谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)和诱导型一氧化氮合酶(inducible nitric oxide synthase iNOS)的活性;Western blot法测大鼠脑组织Bcl-2和Bax两种蛋白的表达水平。结果:红景天苷5、10mg/kg能改善MCAO-I/R大鼠的神经功能(P<0.05,P<0.01);减小脑缺血面积(P<0.05,P<0.01);红景天苷5mg/kg能提高脑内GSH-Px活性(P<0.05);降低iNOS的活性(P<0.05);红景天苷5mg/kg组与模型组Bcl-2的表达分别为(1.54±0.44)、(1.02±0.33),显著增加Bcl-2的表达(P<0.05);Bax表达分别为(1.21±0.12)、(1.44±0.15),红景天苷5mg/kg使Bax的表达显著减少(P<0.01)。结论:红景天苷可以通过增加自由基的清除、调节凋亡和抗凋亡蛋白的表达来减轻MCAO-I/R造成的脑组织损伤。更多还原

【Abstract】 Objective:To explore the protective effects and mechanisms of salidroside on cerebral ischemia-reperfusion injury in middle cerebral artery occlusive(MCAO)rats.Methods:Focal cerebral ischemia in rats was produced by 1.5 h occlusion of the middle cerebral artery and 24 h reperfusion.Salidroside was administered intravenously immediately after occlusion and reperfusion respectively.The neurologic deficit scores were investigated according to Zea-Longa’s Standard.The infarct areas were assessed with software Imagepro Plus 6.0 after TTC staining.And the activities of inducible nitric oxide synthase(iNOS)as well as glutathione peroxidase(GSH-Px)were determined by specific kit.The levels of B cell lymphoma/lewkmia-2(Bcl-2)and Bcl-2 assaciated X protein(Bax)in central neutral system were assessed by western blot.Results:Compared with the model group,salidroside could decrease the neurologic deficit score,reduced the infarct areas of the brain in MCAO-I/R rats,increased the activity of GSH-Px and decreased the activity of iNOS,enhanced the expression of Bcl-2,depressed the expression of Bax.Conclusion:Salidroside has a protective effect on cerebral ischemia-reperfusion injury and this effect is related to attenuating lipid peroxidation,enhancing the expression of Bcl-2 and diminishing Bax expression.更多还原