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目的 研究药理剂量氟美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 健康成年雄性SD大鼠随机分为假手术组、生理盐水组、氟美松组 ,分别对应脑缺血 3h、6h、12h、2 4h、4 8h、72h、12 0h等时间点 ;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 ,氟美松组静脉注射氟美松 ( 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 ;氟美松组细胞凋亡出现时间提前到缺血 1d ,而且缺血 2d、5d凋亡细胞数量较生理盐水组增加 ;脑缺血 3h～ 5h梗死灶边缘区域都有Bcl 2蛋白表达 ;氟美松处理组 6h～ 5dBcl 2蛋白表达细胞密度明显低于生理盐水组。结论 持续性局灶脑缺血早期给予氟美松可促进梗死灶边缘区的细胞凋亡 ,引作用与其下调Bcl 2的基因表达有关
Objective To study the effect of pharmacological dose of dexmedetomidine on apoptosis and the expression of Bcl-2 in adult rats after focal cerebral ischemia. Methods Healthy adult male Sprague-Dawley rats were randomly divided into sham operation group, normal saline group and dexamethasone group, respectively corresponding to time points of 3h, 6h, 12h, 24h, 48h, 72h, 120h, The model of persistent focal cerebral ischemia was established by proximal electrocautery in the side of the middle cerebral artery. The rats in the normal saline group were injected with normal saline at 1 hour after operation, and received 0.950 mg · kg -1 d- 1); routine HE staining, in situ TUNEL labeled apoptotic cells, immunohistochemical detection of Bcl 2 protein expression. Results Bcl-2 protein expression was mainly located in the border area of infarcted area after persistent focal cerebral ischemia. Apoptosis occurred on the 2nd day after ischemia and continued until ischemia for 5 days. The number of apoptotic cells increased at 2d and 5d after ischemia compared with that in saline group. The expression of Bcl-2 protein was detected at 3h-5h after infarction in ischemic area and 6h-5dBcl 2 protein expression Cell density was significantly lower than the saline group. Conclusion: Pretreatment with flumethasone can promote the apoptosis in the border zone of infarcted area, which is related to the down-regulation of Bcl 2 gene expression