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目的 探讨药理剂量地塞米松对成年大鼠持续性局灶脑缺血后凋亡及凋亡相关基因Bcl 2表达的影响。方法 将 10 5只健康成年雄性SD大鼠随机分为假手术组 (7只 )、生理盐水组 (4 9只 )、地塞米松组 (4 9只 ) ,分别对应缺血 3、6、12、2 4、4 8、72、12 0h时间点 (每个时间点组 7只大鼠 )行左侧大脑中动脉近端电凝术 ,建立持续性局灶脑缺血模型。术后 1h生理盐水组静脉注射生理盐水 ,地塞米松组静脉注射地塞米松 (0 .5mg·kg-1·d-1)。行常规HE染色 ,原位末端TUNEL法标记凋亡细胞 ,免疫组织化学法检测Bcl 2蛋白表达。结果 持续性局灶脑缺血后细胞凋亡、Bcl 2蛋白表达主要分布在梗死灶的边缘区域 ,脑缺血 2d出现细胞凋亡并持续到缺血 5d。地塞米松组细胞凋亡出现时间提前到缺血 1d ,而且缺血 2d、5d凋亡细胞数量比生理盐水组增加。脑缺血 3h到 5d梗死灶边缘区域都有Bcl 2蛋白表达。地塞米松处理组 6h到 5dBcl 2蛋白表达细胞密度明显小于生理盐水组。结论 持续性局灶脑缺血早期给予地塞米松可能促进梗死灶边缘区的细胞凋亡 ,此作用与其下调Bcl 2的基因表达有关。
Objective To investigate the effect of dexamethasone on the apoptosis and the expression of Bcl-2 in adult rats after focal cerebral ischemia. Methods A total of 105 healthy adult male Sprague-Dawley rats were randomly divided into sham operation group (n = 7), saline group (n = 9) and dexamethasone group (n = 49) , 2, 4, 8, 72, 120h (7 rats at each time point), the left middle cerebral artery was electrocoagulated and a continuous focal cerebral ischemia model was established. Rats in the normal saline group were injected with normal saline 1 hour after dexamethasone and dexamethasone (0. 5 mg · kg -1 · d -1) intravenously. Normal HE staining, apoptotic cells were labeled by TUNEL in situ and the expression of Bcl2 protein was detected by immunohistochemistry. Results Apoptosis was observed after focal cerebral ischemia. The expression of Bcl-2 protein mainly distributed in the marginal zone of infarction. Apoptosis occurred on the 2nd day after cerebral ischemia and continued to ischemia for 5 days. Dexamethasone group apoptosis appeared ahead of ischemia 1d, and 2d, 5d apoptotic cells increased compared with the saline group. Bcl 2 protein expression was found in the marginal zone of infarct between 3h and 5d after cerebral ischemia. Dexamethasone treatment group 6h to 5dBcl 2 protein expression cell density was significantly lower than the saline group. Conclusion Dexamethasone may promote the apoptosis in the border zone of infarct zone in the early stage of persistent focal cerebral ischemia, which may be related to the downregulation of Bcl 2 gene expression.