红景天苷对缺血再灌注大鼠脑组织损伤的保护作用

Protective effects and mechanisms of salidroside on cerebral ischemia-reperfusion injury

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。

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.