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JAK2-STAT3信号通路在舒芬太尼预处理诱导大鼠心肌保护效应中的作用
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JAK2-STAT3信号通路在舒芬太尼预处理诱导大鼠心肌保护效应中的作用
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Journal Article
JAK2-STAT3信号通路在舒芬太尼预处理诱导大鼠心肌保护效应中的作用
2014
Overview
目的 探讨舒芬太尼预处理对大鼠心肌缺血再灌注损伤的影响以及JAK2-STAT3信号通路的作用.方法 雄性SD大鼠60只,体质量250～300 g,随机均分为假手术组（S组）、缺血再灌注组（I/R组）、舒芬太尼预处理组（SPC组）、舒芬太尼预处理联合JAK2激酶抑制剂组（S＋A组）及JAK2激酶抑制剂组（A组）.采用结扎冠状动脉左前降支的方法制作心肌缺血再灌注模型.SPC组于心肌缺血前股静脉泵注舒芬太尼1μg/kg,泵注5 min,间隔5 min,重复处理3次,总量共3 μg/kg;S＋A组：舒芬太尼预处理前5 min给予JAK2激酶抑制剂AG490（1 mg/kg）,缺血前30min舒芬太尼预处理;A组：缺血前35 min给予JAK2激酶抑制剂AG490（1 mg/kg）.心肌缺血前30min（T0）、缺血前即刻（T1）、缺血30 min（T2）、再灌注30 min（T3）和再灌注120 min（T4）时记录心率（HR）和平均动脉压（MAP）.再灌注120 min抽取动脉血,离心取血清测定肌酸激酶同工酶（CK-MB）和乳酸脱氢酶（LDH）.实验结束时,各组取6只大鼠心脏测算心肌梗死面积,其余6只大鼠采用Western blot测定心肌组织磷酸化STAT3 （P-STAT3）的表达.结果 比较各组间不同时点HR的差异无统计学意义（P＞0.05）.与S组相比,其余各组T2～T4时MAP降低（P＜0.05或P＜0.01）;血清CK-MB和LDH活性明显增高（P＜o.01）.与I/R组相比,SPC组MAP数值稍高,但差异无统计学意义;CK-MB和LDH活性降低（P＜0.01）;心肌梗死范围减小（P＜0.01）.与S组比较,I/R组和SPC组P-STAT3表达上调（P＜0.01）,且SPC组上调高于I/R组（P＜0.01）.结论 舒芬太尼预处理减轻大鼠心肌缺血再灌注损伤的机制可能与激活JAK2-STAT3信号通路、上调P-STAT3的表达有关.
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