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目的:研究防己黄芪汤(FJHQT)对大鼠局灶性脑缺血再灌注(I/R)损伤的保护作用,为其临床防治脑缺血提供实验依据。方法:采用线栓法制备脑缺血再灌注损伤大鼠模型1 d后。将神经行为评分合格的大鼠随机分为FJHQT高、低剂量组、模型组、假手术组和阳性对照尼莫地平组。连续口服给予FJHQT(按生药量计,1,2 g·kg-1)或尼莫地平(2 mg·kg-1)7 d后,观察脑组织的梗死面积,测定脑组织Na+-K+-三磷酸腺苷(Na+-K+-ATP),还原型谷胱甘肽(GSH),过氧化氢酶(CAT)活性及炎症因子白介素-6(IL-6),白介素-1β(IL-1β),肿瘤坏死因子α(TNF-α)水平。采用原位末端标记(TUNEL)法测定脑组织中细胞凋亡,并采用免疫组化和蛋白免疫印迹法(Western blot)分析测定半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)蛋白表达。结果:与正常组比较,模型组大鼠缺血脑组织中Na+-K+-ATP,GSH,CAT活性显著降低(P<0.01),IL-6,IL-1β和TNF-α水平显著提升(P<0.01),凋亡程度及Caspase-3蛋白表达显著提升(P<0.01)。与模型组相比,FJHQT各剂量组均能提高缺血脑组织中Na+-K+-ATP,GSH,CAT活性;降低炎症因子IL-6和TNF-α含量(P<0.05,P<0.01);减轻细胞凋亡程度并降低Caspase-3蛋白表达(P<0.05,P<0.01)。结论:FJHQT能明显减轻缺血脑组织脑梗死面积,减少细胞凋亡、氧化损伤、炎症反应。
Objective: To study the protective effect of FJHQT on focal cerebral ischemia-reperfusion (I / R) injury in rats and provide experimental basis for clinical prevention and treatment of cerebral ischemia. Methods: The rat model of cerebral ischemia-reperfusion injury was established by suture method for one day. The neurobehavioral scores of eligible rats were randomly divided into high and low dose FJHQT group, model group, sham operation group and positive control nimodipine group. After continuous oral administration of FJHQT (1,2 g · kg-1) or nimodipine (2 mg · kg-1) for 7 days, the infarction area of the brain tissue was observed and the content of Na + -K + -ATP (Na + -K + -ATP), reduced glutathione (GSH), catalase (CAT) and interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α) levels. The apoptosis of brain tissue was detected by TUNEL method, and the protein expression of Caspase-3 was detected by immunohistochemistry and Western blot. expression. Results: Compared with normal group, the activity of Na + -K + -ATP, GSH and CAT in model group was significantly decreased (P <0.01) and the levels of IL-6, IL-1β and TNF- <0.01), the degree of apoptosis and the expression of Caspase-3 protein increased significantly (P <0.01). Compared with model group, the FJHQT dose groups could increase the activity of Na + -K + -ATP, GSH and CAT in ischemic brain tissue, decrease the content of IL-6 and TNF-α (P <0.05, P <0.01) Reduce apoptosis and decrease Caspase-3 protein expression (P <0.05, P <0.01). Conclusion: FJHQT can obviously reduce the area of cerebral infarction in ischemic brain tissue, reduce apoptosis, oxidative damage and inflammatory reaction.