中文摘要：

目的观察Apelin-13对大鼠脑缺血-再灌注损伤（CIRI）的保护作用并探讨其机制。方法 50只SD雄性大鼠随机分为假手术组、CIRI模型组及低剂量（0.1μg/kg）、中剂量（1.0μg/kg）和高剂量（10.0μg/kg）Apelin-13处理组。线栓法建立大鼠脑CIRI模型,在缺血2 h后再灌注72 h,Apelin-13处理组于再灌注前30 min侧脑室注射Apelin-13。对各组大鼠神经功能进行评分,TTC染色观察并计算脑梗死体积百分比,Western blot检测损伤侧大脑皮质中内质网应激标志蛋白葡萄糖调节蛋白78（GRP78）和C/EBP同源蛋白（CHOP）的表达。结果与假手术组比较,CIRI模型组大鼠神经功能评分显著增加（P〈0.05）,脑梗死体积百分比达到（47.63±5.81）%;损伤侧大脑皮质中GRP78和CHOP的表达量显著升高（均P〈0.05）。与CIRI模型组相比,低剂量组差异无统计学意义（P〉0.05）;中剂量和高剂量Apelin-13处理组大鼠神经功能缺损明显改善,肌力明显增强,脑梗死体积百分比显著降低,损伤侧大脑皮质中GRP78和CHOP的表达显著降低（均P〈0.05）。结论 Apelin-13对大鼠CIRI有保护作用,其机制可能与抑制内质网应激有关。

英文摘要：

Objective To observe the protective effect of Apelin-13 on the cerebral ischemia-reperfusion injury（CIRI）,and to explore the possible mechanism in rat model.Methods Fifty male SD rats were randomly divided into fivegroups：sham group,CIRI model group and Apelin-13（0.1,1.0 and 10.0 μg/kg） treatment groups.The model of CIRI was es-tablished by filament.After 2 h ischemia,the focal middle cerebral artery was followed by 72 h reperfusion.Apelin-13 wasadministrated by intracerebroventricular injection 30 minutes before reperfusion.The score of neural function was estimatedin different time points.The 2,3,5-triphenyl tetrazolium chloride（TTC） dye was used to calculate the volume and percent-age of cerebral infarction.The endoplasmic reticulum stress（ERS） protein markers including glucose-regulated protein 78（GRP78） and CCAAT/enhancer binding protein homologous protein（CHOP） in cerebral cortex were measured by Westernblot assay.Results Compared with the sham group,the score of neural function was significantly increased,the infarct ratewas reached（47.63 ± 5.81）% and the protein expressions of GRP78 and CHOP were significantly up-regulated in CIRI mod-el group（P〈0.05）.There were no significant differences in these data between the CIRI model group and 0.1 μg/kg Apelin-13 treatment group（P〉0.05）.Compared with the CIRI group,the neural function defect was significantly improved,the mus-cle strength was significantly enhanced and the infarct rate was significantly decreased,and the protein expressions ofGRP78 and CHOP were significantly down-regulated in the 1.0 and 10.0 μg/kg Apelin-13 treatment groups（P〈0.05）.Conclusion Apelin-13 protects the cerebral ischemia-reperfusion injury in rat model,which may be related with the inhibitionof endoplasmic reticulum stress.