防己黄芪汤对脑缺血再灌注模型大鼠脑损伤的保护作用

发布时间：2018-03-21 03:10

本文选题：脑缺血再灌注　切入点：防己黄芪汤　出处：《中国实验方剂学杂志》2015年12期 　论文类型：期刊论文

【摘要】：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(P0.01),IL-6,IL-1β和TNF-α水平显著提升(P0.01),凋亡程度及Caspase-3蛋白表达显著提升(P0.01)。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(P0.05,P0.01);减轻细胞凋亡程度并降低Caspase-3蛋白表达(P0.05,P0.01)。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。
[Abstract]:Objective: to study the protective effect of Fangji Huangqi decoction (FJHQT) on focal cerebral ischemia-reperfusion injury in rats. Methods: after 1 day of cerebral ischemia reperfusion injury, the rats with good neurological behavior were randomly divided into FJHQT high dose group, low dose group and model group. The infarct size of brain tissue was observed after continuous oral administration of FJHQT (2g 路kg-1) or nimodipine (2mg 路kg-1)7 d) in sham operation group and Nimodipine group. The activity of Na K ATPase, reduced glutathione glutathione (GSH), catalase (CAT) and the levels of inflammatory cytokines IL 6, IL 6, IL 1 尾 1 尾, TNF- 伪) in brain tissue were determined by in situ end labeling Tunel (Tunel) method, and the expression of TNF- 伪 in brain tissue was determined by in situ terminal end labeling (Tunel) method, and the levels of interleukin 6 (IL 6), interleukin 1 尾 (IL 1 尾), and tumor necrosis factor 伪 (TNF- 伪) were measured by in situ end labeling (Tunel). The expression of cysteine aspartate protease 3 (caspase-3) was determined by immunohistochemistry and Western blotting. In the model group, the activity of Na -K ATPase GSH cat in ischemic brain tissue decreased significantly, the levels of IL-6 IL-1 尾 and TNF- 伪 increased significantly, and the degree of apoptosis and the expression of Caspase-3 protein increased significantly. Compared with the model group, the activity of Na K ATPase GSH cat in ischemic brain tissue was increased in each dose of FJHQT group. To reduce the content of IL-6 and TNF- 伪 and to reduce the degree of apoptosis and the expression of Caspase-3 protein. Conclusion: FJHQT can significantly reduce the area of cerebral infarction, apoptosis, oxidative injury and inflammatory reaction in ischemic brain tissue.
【作者单位】：江西省医药学校;
【分类号】：R285.5;R-332

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