CAJ | 학술논문

目的评价Janus激酶2/信号转导与转录激活子3(JAK2/STAT3)信号通路在川芎嗪减轻大鼠心肌缺血再灌注损伤中的作用.方法健康成年雄性Wistar大鼠64只,体重250～300 g,采用随机数字表法,将大鼠随机分为4组(n＝ 16):假手术组(S组)、缺血再灌注组(I/R组)、川芎嗪组(T组)和JAK2特异性抑制剂AG490组(AG组).采用结扎左冠状动脉前降支30 min,再灌注120 min的方法制备心肌缺血再灌注损伤模型.S组开胸暴露心脏,左冠状动脉前降支仅穿线；T组于阻断左冠状动脉前降支前20 min静脉注射川芎嗪20 mg/kg; AG组于阻断左冠状动脉前降支前20min静脉注射川芎嗪20 mg/kg,再灌注前5min静脉注射AG490 3 μg/g.再灌注l20 nin时,取下腔静脉血样,测定血清肌酸激酶(CK)及乳酸脱氢酶(LDH)的活性；观察心肌超微结构,计算心肌梗死体积百分比.结果与S组比较,I/R组、T组和AG组血清CK和LDH的活性升高(P<0.01)；与I/R组比较,T组血清CK、LDH活性和心肌梗死体积百分比降低,AG组血清CK、LDH活性降低(P<0.01)；与T组比较,AG组血清CK、LDH活性和心肌梗死体积百分比升高(P<0.05).T组心肌病理学损伤较I/R组和AG组减轻.结论 JAK2/STAT3信号通路参与了川芎嗪减轻大鼠心肌缺血再灌注损伤的作用.
목적 평개Janus격매2/신호전도여전록격활자3(JAK2/STAT3)신호통로재천궁진감경대서심기결혈재관주손상중적작용.방법 건강성년웅성Wistar대서64지,체중250～300 g,채용수궤수자표법,장대서수궤분위4조(n＝ 16):가수술조(S조)、결혈재관주조(I/R조)、천궁진조(T조)화JAK2특이성억제제AG490조(AG조).채용결찰좌관상동맥전강지30 min,재관주120 min적방법제비심기결혈재관주손상모형.S조개흉폭로심장,좌관상동맥전강지부천선；T조우조단좌관상동맥전강지전20 min정맥주사천궁진20 mg/kg; AG조우조단좌관상동맥전강지전20min정맥주사천궁진20 mg/kg,재관주전5min정맥주사AG490 3 μg/g.재관주l20 nin시,취하강정맥혈양,측정혈청기산격매(CK)급유산탈경매(LDH)적활성；관찰심기초미결구,계산심기경사체적백분비.결과 여S조비교,I/R조、T조화AG조혈청CK화LDH적활성승고(P<0.01)；여I/R조비교,T조혈청CK、LDH활성화심기경사체적백분비강저,AG조혈청CK、LDH활성강저(P<0.01)；여T조비교,AG조혈청CK、LDH활성화심기경사체적백분비승고(P<0.05).T조심기병이학손상교I/R조화AG조감경.결론 JAK2/STAT3신호통로삼여료천궁진감경대서심기결혈재관주손상적작용.
Objective To evaluate the role of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in attenuation of myocardial ischemia-reperfusion (I/R) injury by tetramethylpyrazine in rats.Methods Sixty-four healthy male Wistar rats weighing 250-300 g were randomly divided into 4 groups( n ＝ 16 each):sham operation group (group S),myocardial I/R group(group I/R),teramethylpyrazine group (group T) and AG,490( a JAK2 inhibitor) group (group AG).Myocardial I/R was induced by 30 min occlusion of left anterior desecending coronary artery (LAD) followed by 120 min reperfusion in groups I/R,T and A.In groups T and A teramethylpyrazine 20 mg/kg was injected iv 20 min before LAD occlusion.In group A AG490 3 tμg/g was injected iv at 5 min before reperfusion.Blood samples were then taken from inferior vena cava at 120 min of reperfusion for measurement of serum creatine phosphokinase (CK) and lactose dehydrogenase (LDH) activities.Myocardial infarct size was then measured and myocardial tissue was obtained for microscopic examination.Results Serum CK and LDH activities were significantly higher in group I/R than in group S.Pretreatment with tetramethylpyrazine significantly decreased myocardial infarct size and I/R-induced increase in serum CK and LDH activities and histologic damage.The protective effect of tetramethylpyrazine against myocardial 1/R injury was attenuated by postconditioning with AG490.Conclusion JAK2/STAT3 signaling pathway is involved in attenuation of myocardial I/R injury by tetramethyl pyrazine in rats.