颈交感干离断对大鼠脑缺血再灌注损伤内质网应激相关因子的影响  

Effects of transection of cervical sympathetic trunk on endoplasmic reticulum stress related factors in rats after focal cerebral ischemia reperfusion injury

作　　者：赵鹏[1,2] 史忠[1] 周坤[1] 苑爱军 聂鑫 

机构地区：[1]第三军医大学新桥医院急救部 [2]解放军65316部队医院普外科

出　　处：《第三军医大学学报》2010年第22期2361-2364,共4页Journal of Third Military Medical University

基　　金：国家重点基础研究发展计划(973计划;2005CB522605)~~

摘　　要：目的采用颈交感干离断(transection of cervical sympathetic trunk,TCST)方法模拟星状神经节阻滞(stellateganglion block,SGB),观察其对局灶性脑缺血再灌注损伤大鼠皮质区神经元凋亡以及内质网应激相关因子GRP78和CHOP表达的影响。方法健康雄性SD大鼠150只,按随机数字表法分成3组:假手术组(sham组)、再灌注模型组(I/R组)、治疗组(T组),每组50只。用线栓法行大脑中动脉栓塞(MCAO)建立大鼠局灶性脑缺血再灌注损伤模型。治疗组行大脑中动脉栓塞后立即行TCST。应用免疫组化及实时荧光定量PCR方法检测脑缺血再灌注后不同时间点缺血周围区GRP78和CHOP的表达;TUNEL法检测细胞凋亡。结果 I/R组和T组皮质区神经元凋亡指数较sham组显著增高(P<0.01);与I/R组相比,T组再灌注12、24、48、72h凋亡指数明显降低(P<0.05,P<0.01)。I/R组和T组GRP78、CHOPmRNA和蛋白表达较sham组明显上调(P<0.01);与I/R组相比,除72h外,T组6、12、24、48h GRP78、CHOP mRNA和蛋白的表达量明显降低(P<0.05,P<0.01),但仍高于sham组(P<0.05)。结论 TCST对大鼠局灶性脑缺血损伤具有保护作用,其作用机制可能与改善内质网应激状态、降低内质网应激相关凋亡途径,从而发挥抗凋亡作用有关。Objective To investigate the effects of transection of cervical sympathetic trunk （TCST） on neuronal apoptosis and the expressions of endoplasmic reticulum stress （ERS） related factors GRP78 and CHOP after focal cerebral ischemia reperfusion injury by simulating stellate ganglion block. Methods One hundred and fifty male SD rats were randomly divided into 3 groups（n=50）： sham operation, reperfusion model and treatment groups. The models of focal brain ischemia-reperfusion injury was established by occlusion of right middle cerebral artery. The rats in treatment group were performed by TCST after middle cerebral artery occlusion （MCAO）. The expressions of GRP78 and CHOP in the ischemic penumbra tissue was detected by real-time PCR and immunohistochemistry at different time points, 12, 24, 48 and 72 h after 2 hours’ ishemia. Apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated dutp nick end labeling （TUNEL）. Results Compared with the sham group, the index of apoptotic neuron was increased significantly in model group and treatment group （P0.01）, and compared with model group, the index of apoptotic neuron was significantly lower in treatment group （P0.05）. Compared with the sham group, the expressions of GRP78 and CHOP were increased significantly in model group and treatment group （P0.01）, and compared with model group, the index of apoptotic neuron was significantly lower in treatment group （P0.05, P0.01） at different time points 6, 12, 24, 48 h except 72 h after 2 hours’ ischemia. Conclusion TCST has the protective effects against cerebral damage induced by focal ischemia reperfusion in rats, which may be related to inhibiting the process of the neuronal apoptosis. The mechanism of anti-apoptotic effect of TCST may be related to ERS and inhibit the ERS apoptosis pathway.

关 键 词：大脑中动脉栓塞 颈交感干离断 星状神经节阻滞 内质网应激 凋亡 

分 类 号：R741.02[医药卫生—神经病学与精神病学] R741.05[医药卫生—临床医学]