摘要
[目的]探索新型抗炎蛋白分子MCPIP1介导电针治疗急性缺血性脑卒中血脑屏障损害的作用及作用机制。[方法]使用大鼠脑缺血再灌注损伤模型,MCPIP1 knockout及野生型成年雄性小鼠。实验动物分为6组,野生型分3组,分别为假手术组、脑缺血损伤组、脑缺血损伤+电针组;MCPIP1基因敲除(knockout)型分3组,分别为假手术组、脑缺血损伤组、脑缺血损伤+电针组。每组8-10只动物。观察电针对实验动物脑损伤组织肿胀度、血脑屏障通透性、脑组织MMP-9表达水平以及脑组织微血管外周紧密连接蛋白ZO-1水平的影响。[结果]与MCPIP1 knockout动物比较,电针治疗组可以明显减轻野生型动物脑损伤组织肿胀度,降低血脑屏障通透性,抑制MMP-9蛋白表达并且减少脑组织微血管紧密连接蛋白ZO-1的降解,经比较差异均有统计学意义(P<0.05)。[结论]电针可以通过新型抗炎蛋白MCPIP1对缺血脑组织血脑屏障损害起治疗保护作用。
[Objective] The study confirmed that the inhibiting inflammation after brain ischemia is clinically important target for the treatment of stroke injury. The present study sought to determine the involvement of monocyte chemotactic protein-induced protein 1 （MCPIP1） in the cerebral neuroprotection conferred by EA treatment in the animal model of focal cerebral ischemia and to elucidate the mechanisms of EA treatment-induced neuroprotection in the BBB damage.[Method] Focal cerebral ischemia was induced by middle cerebral artery occlusion（MCAO） for 2 hours followed by 3 days reperfusion in male MCPIP1 Knockout（knockout） adult mice and male wild-type adult mice, weighing 23~28g. EA was performed 2 hours after MCAO, twice per day. Experimental animals were divided into six groups：wild type divided into three groups, namely sham group, cerebral ischemic injury group, cerebral ischemic injury ＋ EA group; MCPIP1 knockout type divided into three groups, namely sham group, cerebral ischemia injury group, cerebral ischemic injury ＋ EA group, 8~10 animals per group. Observations of animal brain tissue swelling and damage, blood-brain barrier permeability, MMP-9 expression levels in brain tissue and brain microvascular tight junction protein ZO-1 levels were performed. [Results] Compared with MCPIP1 knockout animals, acupuncture treatment group can significantly reduce wild-type animal brain tissue swelling, inhibit blood brain barrier permeability, reduce MMP-9 protein expression in the brain and inhibit the degradation of brain microvascular tight junction protein ZO-1. [Conclusion] Our data demonstrated that MCPIP1 deficiency caused significant lack of EA treatment-induced cerebral protective effects on BBB damage after MCAO compared with wild type mice and that MCPIP1 was involved in EA treatment-induced neuroprotection on BBB injury after ischemic stroke.
作者
金竹青
周鑫
杜梧榕
金帅捷
张怀波
梁健
Jin Zhuqing Zhou Xin Du Wurong et al(School of Basic Medicine, Zhejiang Chinese Medical University, Hangzhou（310053 The First Affil- iated Hospita of Zhejiartg Chinese. Medical University)
出处
《浙江中医药大学学报》
CAS
2016年第12期870-875,882,共7页
Journal of Zhejiang Chinese Medical University
基金
浙江省自然科学基金项目(LY14H270013)~~
