CAJ | 학술논문

目的评价缺血后处理对大鼠脑缺血再灌注时内质网应激的影响.方法健康雄性SD大鼠90只,体重350 ～ 450 g.采用随机数字表法,将其分为3组(n=30):假手术组(S组)、缺血再灌注组(I/R组)和缺血后处理组(P组).采用阻断左侧大脑中动脉并阻断双侧颈总动脉30 min恢复灌注的方法制备大鼠脑缺血再灌注损伤模型.S组仅分离血管,P组于再灌注即刻行双侧颈总动脉再灌注30 s,缺血10s,重复3次.于再灌注24h时行神经功能缺陷评分,采用TTC法测定脑梗死体积.再灌注6、12、24 h时采用免疫组化法检测缺血侧大脑皮层葡萄糖调节蛋白78 (GRP78)、C/EBP同源蛋白(CHOP)和caspase-12蛋白表达,采用TUNEL法测定神经细胞凋亡情况.结果与S组比较,I/R组和P组神经功能缺陷评分升高、脑梗死体积增大,神经细胞凋亡计数增多,大脑皮层GRP78、CHOP和caspase-12蛋白表达上调(P＜0.05);与I/R组比较,P组神经功能缺陷评分降低,脑梗死体积减小,再灌注12、24 h时大脑皮层GRP78蛋白表达上调,再灌注24h时神经细胞凋亡计数减少,CHOP和caspase-12蛋白表达下调(P＜0.05).结论缺血后处理虽然可抑制大鼠脑缺血再灌注时内质网应激介导的神经细胞凋亡,但该作用在其脑保护中未起主导作用.
목적 평개결혈후처리대대서뇌결혈재관주시내질망응격적영향.방법 건강웅성SD대서90지,체중350 ～ 450 g.채용수궤수자표법,장기분위3조(n=30):가수술조(S조)、결혈재관주조(I/R조)화결혈후처리조(P조).채용조단좌측대뇌중동맥병조단쌍측경총동맥30 min회복관주적방법제비대서뇌결혈재관주손상모형.S조부분리혈관,P조우재관주즉각행쌍측경총동맥재관주30 s,결혈10s,중복3차.우재관주24h시행신경공능결함평분,채용TTC법측정뇌경사체적.재관주6、12、24 h시채용면역조화법검측결혈측대뇌피층포도당조절단백78 (GRP78)、C/EBP동원단백(CHOP)화caspase-12단백표체,채용TUNEL법측정신경세포조망정황.결과 여S조비교,I/R조화P조신경공능결함평분승고、뇌경사체적증대,신경세포조망계수증다,대뇌피층GRP78、CHOP화caspase-12단백표체상조(P＜0.05);여I/R조비교,P조신경공능결함평분강저,뇌경사체적감소,재관주12、24 h시대뇌피층GRP78단백표체상조,재관주24h시신경세포조망계수감소,CHOP화caspase-12단백표체하조(P＜0.05).결론 결혈후처리수연가억제대서뇌결혈재관주시내질망응격개도적신경세포조망,단해작용재기뇌보호중미기주도작용.
Objective To evaluate the ischemic postconditioning on endoplasmic reticulum stress during cerebral ischemia/reperfusion (I/R) in rats.Methods Ninety adult male Sprague-Dawley rats,aged 350-450 g,were randomly divided into 3 groups (n =30 each) using a random number table:sham operation group (S group),I/R group,and ischemic postconditioning group (group P).Focal cerebral I/R was induced by electrocoagulation of left middle cerebral artery and 30 min occlusion of bilateral common carotid arteries followed by reperfusion.In group P,bilateral common carotid arteries were subjected to 3 cycles of 30 s reperfusion and 10 s ischemia at the beginning of reperfusion.At 24 h of reperfusion,neurological deficit was scored,and cerebral infarct size was detected by TTC staining.At 6,12 and 24 h of reperfusion,the expression of glucose-regulated protein 78 (GRP78),C/EBP homologous protein (CHOP) and caspase-12 in the ischemic area were measured (using immunohistochemistry).The neuronal apoptosis in the ischemic area was detected by TUNEL.Results Compared with S group,the neurological deficit score was significantly increased,cerebral infarct size was enlarged,the neuronal apoptosis was increased,and the expression of GRP78,CHOP and caspase-12 was up-regulated in I/R and P groups.The neurological deficit score was significantly lower,cerebral infarct size was smaller,the expression of GRP78 was higher at 12 and 24 h of reperfusion,the neuronal apoptosis was lower at 24 h of reperfusion,and the expression of CHOP and caspase-12 was lower in group P than in group I/R.Concluion Ischemic postconditioning can inhibit neuronal apoptosis mediated by endoplasmic reticulum stress during cerebral I/R,which dose not play a leading role in cerebral protection in rats.