【摘要】： 目的:本研究擬證實(shí)雙萜類(lèi)化合物ST-1預(yù)處理抗大鼠局灶性腦缺血再灌注損傷作用,并通過(guò)對(duì)Bcl-2和NF-κB測(cè)定探討其可能的作用機(jī)制。 方法:健康成年大鼠隨機(jī)分成偽手術(shù)組、缺血再灌注組、ST-1預(yù)處理組(高、中、低劑量組)、尼莫地平陽(yáng)性對(duì)照組,每組30只。依照Koizumi法制作大腦中動(dòng)脈阻斷(MCAO)的腦缺血再灌注模型,缺血2小時(shí)再灌注22小時(shí);觀察再灌注末大鼠行為學(xué)變化、測(cè)定腦梗死體積、腦組織丙二醛(MDA)含量和超氧化物歧化酶(SOD)的活性、觀察腦組織形態(tài)病理學(xué)變化;用免疫組化方法測(cè)定偽手術(shù)組、缺血再灌注組、ST-1預(yù)處理高劑量組的Bcl-2和NF-κB表達(dá)的變化。 結(jié)果:大鼠腦缺血再灌注后引起較大范圍的腦組織的梗死、明顯的神經(jīng)行為學(xué)改變、生化指標(biāo)的改變、病理學(xué)改變以及某些蛋白表達(dá)的變化。ST-1 10、20 mg.kg-1,iv和尼莫地平預(yù)處理可有效減輕腦缺血再灌注損傷:減小腦梗死范圍,改善神經(jīng)行為學(xué)損傷,降低MDA含量、提高SOD活性以及減輕因缺血再灌注引起的組織學(xué)損傷。大鼠腦缺血再灌注可引起B(yǎng)cl-2和NF-κB表達(dá)增加, ST-1 20 mg預(yù)處理增加了缺血再灌注后Bcl-2的表達(dá),降低了NF-κB的表達(dá)。 結(jié)論:ST-1預(yù)處理有抗大鼠局灶性腦缺血再灌注損傷作用,該作用與抗氧自由基有關(guān),也可能與增加Bcl-2表達(dá)和降低NF-κB的表達(dá)有關(guān)。
[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.
【學(xué)位授予單位】：東南大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類(lèi)號(hào)】：R363

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