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目的:研究大鼠局灶性脑缺血后AngⅡ在脑组织中的表达变化规律及应用自由基清除剂-依达拉奉干预治疗对脑组织中AngⅡ表达的影响,探讨脑缺血后脑内AngⅡ表达的生物学作用及依达拉奉对缺血性脑损伤的保护作用。方法:采用微创开颅法建立大鼠大脑中动脉闭塞(MCAO)模型,分为正常对照组、假手术组、脑缺血组和药物干预组。应用免疫组织化学及尼氏染色方法分别观察脑缺血后和依达拉奉干预后AngⅡ在脑内的表达和神经元的变化。结果:在缺血半暗区可见大量AngⅡ阳性细胞,以缺血后1周数目最多,且免疫阳性反应最强,与对照组相比有显著性差异(P<0.05);尼氏染色显示,缺血半暗区可见大量变性坏死神经元,其中以1周组数量最多,与对照组相比有统计学意义(P<0.05);经依达拉奉干预后半暗区AngⅡ阳性细胞数量、光密度值及变性坏死神经元数量明显减少,与对照组比较有统计学差异,以治疗后3 d最为显著(P<0.01)。结论:①大鼠局灶性脑缺血后缺血半暗区AngⅡ表达增强,可能与缺血后神经元的病理变化有一定联系;②脑损伤后,依达拉奉可能通过抑制AngⅡ的表达而减少神经元的坏死,发挥脑保护作用。
Aims: To study the changes of Ang Ⅱ expression in brain tissue after focal cerebral ischemia in rats and the effect of radical scavenging agent-edaravone on the expression of AngⅡ in brain tissue, The biological role of edaravone and the protective effect of edaravone on ischemic brain injury. Methods: The model of middle cerebral artery occlusion (MCAO) in rats was established by minimally invasive craniotomy. The rats were divided into normal control group, sham operation group, cerebral ischemia group and drug intervention group. Immunohistochemistry and Nissl staining were used to observe the expression of AngⅡ and the changes of neurons in cerebral ischemia and edaravone respectively. Results: A large number of AngⅡ positive cells were found in the penumbra area of ischemic area. The number of Ang Ⅱ positive cells was the highest at 1 week after ischemia, and the immunoreactivity was the strongest. Compared with the control group, there was a significant difference (P <0.05) A large number of necrotic neurons were seen in the half-dark ischemic area, with the largest number in the 1-week group and the control group (P <0.05). The number of AngⅡ positive cells in the semi-dark area after edaravone treatment, The number of optical density and the number of degenerative and necrotic neurons decreased significantly compared with the control group, and the difference was statistically significant at 3 days after treatment (P <0.01). Conclusion: ①The expression of AngⅡ in the ischemic penumbra of focal cerebral ischemia in rats may be related to the pathological changes of ischemic neurons; ② Edaravone may inhibit the expression of AngⅡ after cerebral injury And reduce neuronal necrosis, play a protective role in the brain.