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目的 :观察小鼠脑缺血再灌注后海马区基质金属蛋白酶 (MMPs)表达情况 ,探讨其在脑缺血损伤中的作用以及养阴通脑颗粒对脑缺血损伤保护作用的机制。方法 :应用免疫组织化学技术观察脑缺血再灌注后海马区基质金属蛋白酶 9(MMP9)蛋白表达的变化。结果 :模型组缺血再灌注 2 0 min后 CA1区的 MMP9表达明显增加 ,其阳性细胞数平均为 (4 2 .3± 17.1)个 ,与假手术组 (4 .8± 1.6 )个比较有明显差异 (P<0 .0 5 )。养阴通脑颗粒、尼莫地平可使 MMP9表达明显降低 ,其阳性细胞数分别为 (7.2± 2 .9)个和 (12 .7± 5 .3)个 ,与模型组比较 P均 <0 .0 5。结论 :脑缺血再灌注可诱导 CA1区的 MMP9表达增加 ;MMP9表达增加可能是脑缺血再灌注损伤的机制之一 ;养阴通脑颗粒可抑制 MMP9表达 ,对脑缺血再灌注损伤具有保护作用。
Objective: To observe the expression of matrix metalloproteinases (MMPs) in the hippocampus after cerebral ischemia-reperfusion in mice, and to explore its role in cerebral ischemic injury and the protective mechanism of Yangyintongnao Granules on cerebral ischemic injury. METHODS: Immunohistochemical technique was used to observe the expression of matrix metalloproteinase 9 (MMP9) protein in the hippocampus after cerebral ischemia-reperfusion. Results: The expression of MMP9 in the CA1 region was significantly increased in the model group after 20 min ischemia and reperfusion, and the average number of positive cells was (42.3 ± 17.1), which was compared with the sham operation group (4.8 ± 1.6). Significant differences (P<0.05). Yangyintongnao granules and nimodipine significantly reduced the expression of MMP9, with the number of positive cells being (7.2±2.9) and (12.7±5.3), respectively. Compared with the model group, P was less than 0. .0 5. Conclusion: Cerebral ischemia-reperfusion can induce the expression of MMP9 in CA1 region. The increased expression of MMP9 may be one of the mechanisms of cerebral ischemia-reperfusion injury. Yangyintongnao Granule can inhibit the expression of MMP9 and has the effects on cerebral ischemia reperfusion injury. Protective effects.