氯化钴预处理对全脑缺血再灌注大鼠SDF-1α/CXCR4的表达及对细胞凋亡的影响  

Effect of CoCl_2 preconditioning on the expression of SDF-1α/ CXCR4 and cellular apoptosis in cerebral ischemia reperfusion rats

作　　者：刘春景[1] 张春阳[1] 孙原[1] 李艳玲[1] 石秋艳[1] 

机构地区：[1]河北联合大学附属医院神经内科,河北唐山063000

出　　处：《中风与神经疾病杂志》2015年第4期299-302,共4页Journal of Apoplexy and Nervous Diseases

基　　金：河北省卫生厅资助项目(No.ZL20140185)

摘　　要：目的通过观察缺血再灌注后大鼠海马区SDF-1α/CXCR4表达的变化,观察细胞凋亡探讨缺血缺氧环境中SDF-1α/CXCR4生物轴的脑保护作用及氯化钴预处理的影响。方法将130只成年雄性SD大鼠随机分为正常对照组(n=5)、假手术组(n=5)、模型组(脑缺血组,n=60)、干预组(氯化钴组,n=60)。按缺血后再灌注时间不同分为再灌注2 h、6 h、12 h、24 h、48 h、72 h 6个亚组。采用四血管阻断法制备大鼠全脑缺血再灌注模型,通过免疫组化法观察脑缺血后再灌注各个时间点海马区SDF-1α及CXCR4的表达变化,TUNEL法观察各组不同时间点细胞凋亡的差异。结果免疫组化:模型组及干预组SDF-1α、CXCR4的阳性表达均高于假手术组,模型组于脑缺血再灌注6 h海马区SDF-1α、CXCR4阳性细胞表达明显增加,48 h表达至各时间点最高水平,随后表达逐渐减少,72 h仍有阳性表达。干预组各时间点海马区SDF-1α、CXCR4的阳性细胞表达均高于对照组,差异有统计学意义(P<0.05)。TUNEL:与模型组比较,干预组凋亡指数低于模型组(P<0.05)。结论氯化钴可能通过上调SDF-1α、CXCR4的表达,诱导脑缺氧耐受,促进干细胞向缺血组织迁移,间接发挥脑保护作用。Objective By observing the hippocampus of rats after ischemia-reperfusion SDF-1α / CXCR4 expression changes,to observe the apoptosis of ischemia hypoxia environment of SDF-1α / CXCR4 biological axis of brain protection and the effect of cobalt chloride pretreatment. Methods 120 adult male SD rats were randomly divided into normal control group（ n = 5）,Sham group（ n = 5）,model group,ischemic group（ n = 60）,intervention group（ cobalt chloride group（ n =60）. According to the different divided into reperfusion after ischemia reperfusion time rats were divided into 2 h,6 h,12 h,24 h,48 h,72 h 6 subgroups. Using four vascular block prepared full brain ischemia reperfusion model,rats SDF-1α and CXCR4 expression in the hippocampus were observed by immunohistochemical method to observe the cerebral ischemia reperfusion after various points in the hippocampus of SDF-1α and CXCR4 expression changes. Results Immunohistochemistry： SDF-1α,CXCR4 expression in Mmodel group and intervention group SDF-1α,CXCR4 expression was were higher than the sham group,SDF-1α and CXCR4-positive cells in hippocampus of 6 h reperfusion model group hippocampus SDF-1α in cerebral ischemia,CXCR4-positive cells was were significantly increased,48 h the expression to was the highest level in 48 h after reperfusion level at each time point,and then expression gradually decreased expression,72 h isit was still positive at 72 h. SDF-1α,CXCR4 positive cells of i Intervention group at each time point in the hippocampus SDF-1α,CXCR4 positive cells were higher,the difference was statistically significant（ P〈0. 05）. TUNEL： compared with model group,intervention group apoptosis index is was lower than the model group（ P〈0. 05）. Conclusion Cobalt chloride may promote the migration of stem cells to ischemic tissue,indirectly play a role of brain protection be through the ischemic tolerance by upregulation of SDF-1α and,the expression of CXCR4,lack of tolerance induction,promote the migration of stem cells to ischemic

关 键 词：全脑缺血再灌注 氯化钴 SDF-1Α CXCR4 凋亡 

分 类 号：R743.3[医药卫生—神经病学与精神病学]