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目的:观察TanⅡA干预缺血-再灌注(I/R)大鼠脑组织病理学特征的变化,以及NF-κB、ⅠκB的表达,研究TanⅡA对血管性痴呆的影响及其作用机理。方法:将80只大鼠随机分为正常对照组、假手术组、缺血-再灌注7d和15 d模型组及TanⅡA低、高剂量7 d和15 d组,每组10只。TanⅡA低剂量组(4 mg/kg)和高剂量组(8 mg/kg)分别于术后连续腹腔注射给药7 d和15 d,1次/d,假手术组和模型组给予等体积生理盐水腹腔注射。后用HE染色观察大脑组织的病理学变化,免疫组织化学染色法检测TanⅡA处理后各组NF-κB和IκB表达水平的改变。结果:TanⅡA组脑组织病变程度较MCAO模型组有不同程度减轻,其中以15 d高剂量组改变最为明显,免疫组化结果也显示模型组的NF-κB和IκB表达水平在显著高于TanⅡA组和正常对照组(P<0.05)。结论:TanⅡA能有效降低缺血-再灌大鼠模型脑组织NF-κB和IκB蛋白的表达水平,其机制可能是通过抑制NF-κB和IκB的活性和生成有效的降低大脑中炎性反应的发生,从而发挥保护大脑神经元,改善缺血-再灌脑组织损伤的作用。
OBJECTIVE: To observe the changes of brain histopathological changes and the expression of NF-κB and IκB induced by TanⅡA in rats after ischemia-reperfusion (I / R), and to study the effect of TanⅡA on vascular dementia and its mechanism. Methods: Eighty rats were randomly divided into normal control group, sham operation group, model group on the 7th day and 15th day after ischemia - reperfusion and low and high dose TanIIA group on the 7th and 15th day. The rats in TanⅡA low dose group (4 mg / kg) and high dose group (8 mg / kg) were given intraperitoneal injection for 7 days and 15 days, once per day respectively. The sham operation group and model group were given equal volume of physiology Saline intraperitoneal injection. The pathological changes of brain tissue were observed with HE staining. The expression of NF-κB and IκB in each group was detected by immunohistochemical staining. Results: Compared with MCAO model group, the degree of brain lesions in TanⅡA group was alleviated to a lesser extent, especially in 15-day high dose group. The results of immunohistochemistry also showed that the expression of NF-κB and IκB in TanⅡA group was significantly higher than that in TanⅡA group And normal control group (P <0.05). Conclusion: TanⅡA can effectively reduce the expression of NF-κB and IκB in the brain tissue of rats with ischemia-reperfusion. Its mechanism may be through inhibiting the activity of NF-κB and IκB, and effectively reducing the inflammatory reaction in the brain Occurrence, thus play a role in protecting brain neurons, improve tissue damage of ischemia - reperfusion brain.