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目的探讨银杏内酯B对大脑局灶性缺血再灌注模型大鼠的保护作用及可能的机制。方法采用栓线法大鼠缺血3 h再灌注21 h模型,观察银杏内酯B对模型大鼠神经症状、梗死范围及脑组织匀浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSH-PX)、钠-钾ATP酶(Na+-K+-ATPase)、钙-镁ATP酶(Ca2+-My2+-ATPase)活性及丙二醛(MDA)、过氧化氢酶(CAT)、谷胱甘肽(GSH)、一氧化氮(NO)含量的影响。结果银杏内酯B注射液8、4 mg/kg组可明显改善大鼠神经症状,减轻梗塞程度,抑制率分别为29.6%、23.4%(与模型组比较P<0.01,P<0.05)。银杏内酯B注射液8、4 mg/kg可明显升高缺血再灌侧大脑的SOD、GSH-PX活性,提高GSH、CAT含量,降低MDA、NO含量,明显升高缺血再灌侧大脑的Na+-K+-ATPase、Ca2+-My2+-ATPase的活性(P<0.05,P<0.01)。结论银杏内酯B对局灶性脑缺血再灌注损伤大鼠具有保护作用,本作用与银杏内酯B减少大鼠脑缺血再灌注后脑组织NO含量、抗自由基损伤以及改善能量代谢有关。
Objective To investigate the protective effect of ginkgolide B on rat model of focal cerebral ischemia-reperfusion and its possible mechanism. METHODS: Rat model of rat ischemic 3h and reperfusion was used for 21h. The effect of ginkgolide B on neurological symptoms, infarct size, and superoxide dismutase (SOD) and glutathione in brain homogenate were observed. GSH-PX, Na+-K+-ATPase, Ca2+-My2+-ATPase activity and malondialdehyde (MDA), catalase (CAT), Effects of glutathione (GSH) and nitric oxide (NO) content. RESULTS: Ginkgolide B injection in the 8 and 4 mg/kg groups significantly improved neurological symptoms and reduced infarct size. The inhibition rates were 29.6% and 23.4%, respectively (P<0.01, P<0.05 compared with the model group). Ginkgolide B injection 8, 4 mg/kg can significantly increase the activity of SOD and GSH-PX in the brain of the ischemic reperfusion, increase the content of GSH and CAT, decrease the content of MDA and NO, and significantly increase the level of ischemia and reperfusion. Na+-K+-ATPase and Ca2+-My2+-ATPase activity in the brain (P<0.05, P<0.01). Conclusion Ginkgolide B has a protective effect on focal cerebral ischemia-reperfusion injury in rats. This effect is related to the decrease of NO content, anti-free radical injury and improvement of energy metabolism after cerebral ischemia-reperfusion in rats with ginkgolide B. .