ST-1抗大鼠局灶性脑缺血再灌注损伤作用

发布时间：2018-10-08 17:23

【摘要】： 目的:本研究拟证实双萜类化合物ST-1预处理抗大鼠局灶性脑缺血再灌注损伤作用,并通过对Bcl-2和NF-κB测定探讨其可能的作用机制。方法:健康成年大鼠随机分成伪手术组、缺血再灌注组、ST-1预处理组(高、中、低剂量组)、尼莫地平阳性对照组,每组30只。依照Koizumi法制作大脑中动脉阻断(MCAO)的脑缺血再灌注模型,缺血2小时再灌注22小时;观察再灌注末大鼠行为学变化、测定脑梗死体积、脑组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)的活性、观察脑组织形态病理学变化;用免疫组化方法测定伪手术组、缺血再灌注组、ST-1预处理高剂量组的Bcl-2和NF-κB表达的变化。结果:大鼠脑缺血再灌注后引起较大范围的脑组织的梗死、明显的神经行为学改变、生化指标的改变、病理学改变以及某些蛋白表达的变化。ST-1 10、20 mg.kg-1,iv和尼莫地平预处理可有效减轻脑缺血再灌注损伤:减小脑梗死范围,改善神经行为学损伤,降低MDA含量、提高SOD活性以及减轻因缺血再灌注引起的组织学损伤。大鼠脑缺血再灌注可引起Bcl-2和NF-κB表达增加, ST-1 20 mg预处理增加了缺血再灌注后Bcl-2的表达,降低了NF-κB的表达。结论:ST-1预处理有抗大鼠局灶性脑缺血再灌注损伤作用,该作用与抗氧自由基有关,也可能与增加Bcl-2表达和降低NF-κB的表达有关。
[Abstract]:Aim: this study was to confirm the protective effect of ST-1 preconditioning on focal cerebral ischemia-reperfusion injury in rats, and to explore the possible mechanism of Bcl-2 and NF- 魏 B measurement. Methods: healthy adult rats were randomly divided into pseudo-operation group, ischemia reperfusion group, ST-1 preconditioning group (high, middle and low dose groups) and nimodipine positive control group (30 rats in each group). The cerebral ischemia-reperfusion model with middle cerebral artery occlusion of (MCAO) was made according to Koizumi method. The behavioral changes of rats at the end of reperfusion were observed and the infarct volume was measured after 2 hours of ischemia and 22 hours of reperfusion. The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in brain tissue were observed, and the expression of Bcl-2 and NF- 魏 B in high-dose preconditioning group were determined by immunohistochemical method. Results: cerebral ischemia and reperfusion resulted in a large range of cerebral infarction, obvious neurobehavioral changes and biochemical changes. Pathological changes and changes of protein expression. ST-1 10 + 20 mg.kg-1,iv and nimodipine can effectively reduce cerebral ischemia-reperfusion injury, reduce cerebral infarct size, improve neurobehavioral injury, and decrease MDA content. Increase the activity of SOD and alleviate the histological injury caused by ischemia and reperfusion. The expression of Bcl-2 and NF- 魏 B was increased after cerebral ischemia-reperfusion in rats. ST-1 20 mg pretreatment increased the expression of Bcl-2 and decreased the expression of NF- 魏 B after ischemia-reperfusion. Conclusion the effects of 1: ST-1 preconditioning on focal cerebral ischemia-reperfusion injury in rats may be related to the anti-oxygen free radicals, the increase of Bcl-2 expression and the decrease of NF- 魏 B expression.
【学位授予单位】：东南大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R363

【参考文献】