文章摘要
戴伟娟,朱凡河,张国安,徐旭东,王旭.前列腺素E1对大鼠全脑缺血-再灌注损伤细胞凋亡及Caspase-3表达的影响[J].济宁医学院学报,2017,40(2):98-102
前列腺素E1对大鼠全脑缺血-再灌注损伤细胞凋亡及Caspase-3表达的影响
Effects of PGE1 on the apoptosis and expression of caspase-3 in rats with cerebral ischemia-reperfusion injury
投稿时间:2017-03-09  
DOI:10.3969/j.issn.1000-9760.2017.02.005
中文关键词: 前列腺素E1;脑缺血-再灌注;细胞凋亡;半胱氨酸天冬氨酸蛋白酶3
英文关键词: Prostaglandin E1;Rat;Cerebral ischemia-reperfusion;apoptosis;Caspase-3
基金项目:山东省自然科学基金项目(2012ZRB14146)
作者单位
戴伟娟 济宁医学院基础医学院, 济宁 272067 
朱凡河 济宁医学院基础医学院, 济宁 272067 
张国安 济宁医学院基础医学院, 济宁 272067 
徐旭东 济宁医学院基础医学院, 济宁 272067 
王旭 济宁医学院基础医学院, 济宁 272067 
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中文摘要:
      目的 探讨前列腺素E1(PGE1)对大鼠全脑缺血-再灌注损伤神经元凋亡和半胱氨酸天冬氨酸蛋白酶3 (Caspase-3)表达的影响。方法 将健康雄性Wistar大鼠24只,随机分为3组:假手术组、缺血-再灌模型组、PGE1组(12μg/kg),药物于缺血前5mins静脉滴注,持续2h;利用双侧颈总动脉结扎法建立大鼠全脑缺血-再灌注模型,形态学方法观察细胞凋亡的变化,免疫组化染色方法检测脑组织Caspase-3,表达的变化。结果 缺血20mins,再灌注6h后,缺血-再灌模型大鼠脑组织细胞凋亡数和Caspase-3的表达,较假手术组明显增多(P <0.05),与缺血-再灌注模型组相比,PGE1组能减少细胞凋亡的数量,抑制Caspase-3的表达(P <0.05)。结论 PGE1脑保护作用机制与其抑制神经细胞凋亡和Caspase-3表达有关。
英文摘要:
      Objective To investigate the effects of Prostaglandin E1(PGE1) on the neuronal apoptosis and expression of caspase-3 in rats with whole brain ischemia-reperfusion injury.Methods 24 healthy male Wistar rats were randomly divided into three groups which were sham operated group (n=8),cer ebral ischemia-reperfusion model group(n=8).PGE1-pretreated groups (12μg/kg,n=8).Rats model of whole cerebral ischemia-reperfusion injury were made through bilateral common carotid artery ligation for 20min followed with 6 hours of reperfusion.The change of cellular apoptosis were observed with morphological method,and the expression of caspase-3 were detected using immunohistochemical method.Results After the ischemia for 20 min and reperfusion for 6 hin rats,the number of apoptotic cells and the expressions of caspase-3 in brain tissue were increased compared with those in the sham operative group (P <0.01).In PGE1 group,the number of apoptosis cells and the expressions of caspase-3 were lower than those in the isehemia reperfusion model group (P <0.01).Conclusion The protective mechanism of PGE1 on cerebral ischemia-reperfusion injury is related to reducing neuronal apoptosis by inhibiting the expression of caspase-3.
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