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目的:观察丹参酮ⅡA(TanⅡA)对不同时期缺血-再灌注(I/R)的大鼠脑组织GFAP、ATPase与PDI表达的影响,探讨TanⅡA对I/R脑组织的神经保护作用及其分子机理。方法:线栓法建立局灶性脑缺血-再灌注模型,本实验采用64只雄性SD大鼠随机分为假手术组,I/R模型3、7、15 d组及丹参酮ⅡA高、低剂量7、15 d组,实验完成后观察各组脑组织病理学变化,同时用免疫组化法检测脑组织神经胶质原纤维酸性蛋白质(GFAP)、三磷酸腺苷酶(ATPase)及蛋白质二硫化异构酶(PDI)的表达水平。结果:(1)TanⅡA高、低剂量干预7、15 d组脑组织缺血损伤病理学改变明显改善,TanⅡA高剂量组与I/R模型组相比更为显著。(2)I/R模型组GFAP表达增加,TanⅡA高剂量7 d与15 d组和模型组相比较,脑组织GFAP阳性反应显著减弱(P<0.05),TanⅡA高、低剂量组间比较差异无统计学意义(P>0.05)。(3)TanⅡA干预组脑组织ATPase与PDI表达增强,TanⅡA高剂量组与I/R模型组比较更为显著(P<0.05)。结论:TanⅡA通过抑制GFAP的产生,减轻了由过量胶质细胞产生的脑组织炎性反应,同时上调神经元内ATPase与PDI的表达,改善脑缺氧所致的能量代谢障碍,维持细胞内环境稳定,从而起到对I/R脑损伤的神经保护作用。
Objective: To observe the effects of TanⅡA on the expression of GFAP, ATPase and PDI in rat brain after ischemia-reperfusion (I / R) at different periods and to explore the neuroprotective effect of TanⅡA on I / R brain and its molecular mechanism. Methods: Focal cerebral ischemia-reperfusion model was established by thread occlusion. Sixty-four male Sprague-Dawley rats were randomly divided into sham operation group, I / R model 3,7,15 d group and tanshinone Ⅱ A high and low The rats in the 7 and 15 d groups were sacrificed and the histopathological changes in each group were observed after the completion of the experiment. The levels of glial fibrillary acidic protein (GFAP), adenosine triphosphatase (ATPase) and protein disulfide isoforms Enzyme (PDI) expression levels. Results: (1) Pathological changes of ischemic injury of brain tissue in TanⅡA high and low dose intervention groups were significantly improved after 7 and 15 days of intervention. Tan Ⅱ A high dose group was more significant than I / R model group. (2) The expression of GFAP increased in I / R model group, and the positive reaction of GFAP in brain tissue was significantly weaker (P <0.05) on the 7th day and the 15th day in TanⅡA group compared with the model group Statistical significance (P> 0.05). (3) The expression of ATPase and PDI in TanⅡA-treated group increased significantly compared with that in I / R model group (P <0.05). Conclusion: TanⅡA can reduce the inflammatory response induced by glial cells by up-regulating the expression of ATPase and PDI in neurons, inhibiting the energy metabolism disorder induced by hypoxia and maintaining the intracellular environment Stable, and thus play a neuroprotective effect on I / R brain injury.