CAJ | 학술논문

目的评价Janus激酶2-信号转导与转录激活子(JAK2- STAT3)通路在舒芬太尼后处理减轻犬心肌缺血再灌注损伤中的作用.方法健康杂种家犬24只,雌雄不拘,体重10～15 kg,采用随机数字表法,将其随机分为4组(n=6):假手术组(S组)；心肌缺血再灌注损伤组(I/R组),结扎左冠状动脉前降支30 min,再灌注120 min；舒芬太尼后处理组(PO组),再灌注前5min时经5 min静脉输注舒芬太尼0.6 μg/kg；舒芬太尼后处理+AG490组(AG组),再灌注前5min时静脉注射JAK2抑制剂AG490 1 mg/kg后经5 min静脉输注舒芬太尼0.6 μg/kg.于再灌注120 min时取缺血部位心肌标本,光镜下观察病理学结果,采用免疫组化法测定心肌细胞caspase-3和磷酸化STAT3(p- STAT3)的表达,采用TUNEL法测定心肌细胞凋亡指数.结果与S组比较,I/R组、PO组和AG组心肌细胞凋亡指数、caspase-3及p-STAT3的表达均升高(P＜0.05)；与I/R组比较,PO组和AG组心肌细胞凋亡指数和caspase-3表达降低,PO组p-STAT3表达升高,AG组p-STAT3表达降低(P＜0.05)；与PO组比较,AG组心肌细胞凋亡指数和caspase-3表达升高,p-STAT3表达降低(P＜0.05).PO组心肌病理学损伤较I/R组和AG组减轻.结论 JAK2-STAT3通路参与了舒芬太尼后处理减轻犬心肌缺血再灌注损伤.
목적 평개Janus격매2-신호전도여전록격활자(JAK2- STAT3)통로재서분태니후처리감경견심기결혈재관주손상중적작용.방법 건강잡충가견24지,자웅불구,체중10～15 kg,채용수궤수자표법,장기수궤분위4조(n=6):가수술조(S조)；심기결혈재관주손상조(I/R조),결찰좌관상동맥전강지30 min,재관주120 min；서분태니후처리조(PO조),재관주전5min시경5 min정맥수주서분태니0.6 μg/kg；서분태니후처리+AG490조(AG조),재관주전5min시정맥주사JAK2억제제AG490 1 mg/kg후경5 min정맥수주서분태니0.6 μg/kg.우재관주120 min시취결혈부위심기표본,광경하관찰병이학결과,채용면역조화법측정심기세포caspase-3화린산화STAT3(p- STAT3)적표체,채용TUNEL법측정심기세포조망지수.결과 여S조비교,I/R조、PO조화AG조심기세포조망지수、caspase-3급p-STAT3적표체균승고(P＜0.05)；여I/R조비교,PO조화AG조심기세포조망지수화caspase-3표체강저,PO조p-STAT3표체승고,AG조p-STAT3표체강저(P＜0.05)；여PO조비교,AG조심기세포조망지수화caspase-3표체승고,p-STAT3표체강저(P＜0.05).PO조심기병이학손상교I/R조화AG조감경.결론 JAK2-STAT3통로삼여료서분태니후처리감경견심기결혈재관주손상.
Objective To investigate the role of Janus kinese 2-signal transducer and activator of transcription 3 (JAK2-STAT3) pathway in reduction of myocardial ischemia-reperfusion (I/R) injury by sufentanil postconditioning in dogs.Methods Twenty-four healthy dogs of either sex,weighing 10-15 kg,were randomly divided into 4 groups (n =6 each):sham operation group (group S); I/R group; sufentanil postconditioning group (group PO) and sufentanil postconditioning + specific JAK2 inhibitor AG490 group (group AG).In groups I/R,PO and AG,myocardial I/R was produced by occlusion of left anterior descending coronary artery for 30 min followed by 120 min reperfusion.In groups PO and AG,sufentanil 0.6 μg/kg was infused intravenously over 5 min before reperfusion and in addition in group AG,AG490 1 mg/kg was injected intravenously before sufentanil infusion.Myocardial specimens were taken at the end of 120 min reperfusion for microscopic examination and determination of the expression of caspase-3 and p-STAT3 by immuno-histochemistry and myocardial cell apoptosis index (AI) by TUNEL.Results AI and the expression of caspase-3 and p-STAT3 were significantly higher in groups I/R,PO and AG than in group S ( P ＜ 0.05).Compared with group I/R,AI and the expression of caspase-3 were significantly decreased in groups PO and AG,the expression of p-STAT3 was significantly increased in group PO,and the expression of p-STAT3 was significantly decreased in group AG ( P ＜ 0.05).AI and the expression of caspase-3 were significantly higher and the expression of p-STAT3 was significantly lower in group AG than in group PO (P ＜ 0.05).The pathologic changes were significantly attenuated in group PO compared with groups I/R and AG.Conclusion JAK2-STAT3 pathway is involved in reduction of myocardial I/R injury by sufentanil postconditioning in dogs.