摘要
目的:研究Apelin-13对缺血/再灌注小鼠脑损伤的作用,并初步探讨其对自噬性细胞死亡的影响。方法:取健康雄性CD-1小鼠,随机分为假手术(sham)组、生理盐水(Saline)组、Apelin组;Apelin组和Saline组首先建立脑缺血再灌注(MCAO/R)模型,再灌注即刻给予同侧侧脑室注射Apelin-13或等量生理盐水,然后在再灌注48 h后,进行神经功能方面检测,同时利用2,3,5-氯化三苯基四氮唑(TTC)染色评估脑梗死体积;缺血再灌注24 h和48 h后,采用West-blot法检测各组自噬相关蛋白LC3的表达情况。结果:Apelin-13可显著降低小鼠脑缺血再灌注后神经功能缺损症状,减少脑梗死体积,减低自噬相关蛋白LC3的表达及LC3-Ⅱ/LC3-Ⅰ的比值。结论:Apelin-13对小鼠脑缺血再灌注损伤有一定的保护作用,抑制神经细胞的自噬性死亡可能是其作用机制之一。
Objective：To observe the effect of apelin-13 on the brain injury induced by middle cerebral artery occlusion-reperfusion（MCAO/R）,and to explore the relationship between apelin-13 and autophagy in MCAO/R.Method：A total of 48 mice were randomly divided into sham,saline and apelin-13 groups.Firstly, mice s MCAO/R model was established using the suture’s method.After MCAO/R, Apelin-13 and saline groups were pretreated with an immediate injection of Apelin-13 and saline into the mice brain lateral ventricle.The effect of neurological deficit scores and the cerebral infarct volume was measured with TTC at 48h after MCAO/R.At last, to determine the role of Apelin-13 on the brain injury induced by MCAO/R,the autophagy associated proteins LC3 were also assessed with western-bloting.Result：Apelin-13 can significantly decreased neural dysfunction and cerebral infarct volume of mice after MCAO/R 48 h.Inadditionally,Apelin-13 also reduce the amount of protein LC3 expression and down-regulated protein LC3-Ⅱ/LC3-Ⅰratio,at 24 h and 48 h after MCAO/R.Conclusion：Apelin-13 preconditioning has obvious protective effect on mice after MCAO/R,and the mechanism may possibly by suppressing neuron autophagy.
出处
《中国医学创新》
CAS
2016年第20期18-21,共4页
Medical Innovation of China
基金
国家自然科学青年基金项目(81302612)
江苏省高校自然指导项目(15KJD180003)
