CAJ | 학술논문

目的探讨Noah信号通路在电针预处理诱导大鼠脑缺血耐受中的作用.方法健康成年雄性SD大鼠52只,体重280～320 g,随机分为2组(n=26):正常对照组(C组)不做任何处理;电针预处理组(EA组)于百会穴进行电针刺激(刺激条件:疏密波2/15Hz,电流强度1 mA),30 min次,1次/d,连续5 d.最后一次电针刺激结束后24 h采用阻断单侧大脑中动脉120 min再灌注72 h的方法制备局灶性脑缺血再灌注模型.分别于缺血前即刻、再灌注24 h及再灌注72 h时采用Western blot法测定缺血侧大脑皮层Notch细胞内片段(NICD)蛋白的表达,采用实时定量PCR法测定缺血侧大脑皮层Notch通路信号分子的表达;于再灌注72 h时进行神经功能损伤评分,评分完毕后测定脑梗死体积百分比.结果缺血前即刻两组大脑皮层Hesl mRNA及NICD蛋白表达差异无统计学意义(P>0.05);与缺血前即刻比较,两组再灌注24、72 h时NICD蛋白表达上调,C组再灌注72 h时Hesl mRNA 表达上调,EA组再灌注24 h时Hesl mRNA表达上调(P<0.05);与再灌注24 h时比较,再灌注72 h时C组Hesl mRNA及NICD蛋白表达均上调,EA组Hesl mRNA及NICD蛋白表达均下调(P<0.05);与C组比较,EA组缺血前即刻Notchl mRNA、Notch4 mRNA及Jagl mRNA的表达上调,再灌注24 h时Hesl mRNA及NICD蛋白表达上调,再灌注72 h时Hesl mRNA及NICD蛋白表达下调,脑梗死体积百分比降低,神经功能损伤评分升高(P<0.05).结论 Notch信号通路可能参与了电针预处理诱导的大鼠脑缺血耐受.
목적 탐토Noah신호통로재전침예처리유도대서뇌결혈내수중적작용.방법 건강성년웅성SD대서52지,체중280～320 g,수궤분위2조(n=26):정상대조조(C조)불주임하처리;전침예처리조(EA조)우백회혈진행전침자격(자격조건:소밀파2/15Hz,전류강도1 mA),30 min차,1차/d,련속5 d.최후일차전침자격결속후24 h채용조단단측대뇌중동맥120 min재관주72 h적방법제비국조성뇌결혈재관주모형.분별우결혈전즉각、재관주24 h급재관주72 h시채용Western blot법측정결혈측대뇌피층Notch세포내편단(NICD)단백적표체,채용실시정량PCR법측정결혈측대뇌피층Notch통로신호분자적표체;우재관주72 h시진행신경공능손상평분,평분완필후측정뇌경사체적백분비.결과 결혈전즉각량조대뇌피층Hesl mRNA급NICD단백표체차이무통계학의의(P>0.05);여결혈전즉각비교,량조재관주24、72 h시NICD단백표체상조,C조재관주72 h시Hesl mRNA 표체상조,EA조재관주24 h시Hesl mRNA표체상조(P<0.05);여재관주24 h시비교,재관주72 h시C조Hesl mRNA급NICD단백표체균상조,EA조Hesl mRNA급NICD단백표체균하조(P<0.05);여C조비교,EA조결혈전즉각Notchl mRNA、Notch4 mRNA급Jagl mRNA적표체상조,재관주24 h시Hesl mRNA급NICD단백표체상조,재관주72 h시Hesl mRNA급NICD단백표체하조,뇌경사체적백분비강저,신경공능손상평분승고(P<0.05).결론 Notch신호통로가능삼여료전침예처리유도적대서뇌결혈내수.
Objective To investigate the role of Notch signaling pathway in cerebral ischemic tolenmce induced by clectroacupuncture (EA) preconditioning.Methods Fifty-two adult male SD rats weighing 280-320 g were randomly divided into 2 groups(n=each):control group(group C)and electroacupuncture preconditionig group(group EA).Group C received no treatment.Group EA received EA at the Baihui acupoint (GV20) for 30 min a day for 5 days.Twenty-four hours after the last preconditionig,focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 120 min,followed by 72 h of reperfusion.Notch intracellular domain(NICD)expression was determined by Western blot and expression of Notch1,Notch4,Jag1,and Hes1 mRNA by real-time PCR immediately before iachemia and 24 and 72 h of reperfusion.The neurological deficit was scored at 72 h of reperfusion.The infarct volumes were then determined after evaluation of the neurological deficit score .Results There was no significant difference in Hesl mRNA and NICD expression immediately before ischemia between group EA and C(P>O.05).NICD expression was up-regulated at 24 and 72 h of reperfusion in both groups, and Hesl mRNA expression at 72 h of reperfusion in group C and at 24 h of reperfusion in group EA was up-regulated compared with those immediately before ischemia (P < 0.05). Hes1 mRNA and NICD expression was up-regulated in group C, while down-regulated in group EA at 72 h of reperfusion compared with those at 24 h of reperfusion ( P < 0.05 ). Compared with group C, the expression of Notchl,Notch4 and Jag1 mRNA was up-regulated immediately before ischemia, and Hes1 mRNA and NICD expression was up-regulated at 24 h of reperfusion while down-regulated at 72 h of reperfusion in group EA( P < 0.05). EA preconditioning significantly reduced infarct volumes and increased neurological deficit scores at 72 h of reperfusion (P < 0.05 ). Conclusion Notch signaling pathway may participate in cerebral ischemic tolerance induced by EA preconditioning.