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| PI3K/Akt 信号通路在舒芬太尼后处理减轻在体大鼠心肌缺血-再灌注损伤中的作用 |
| Role of PI3K/Akt signaling pathway in the sufentanil postconditioning alleviated myocardial ischemia reperfusion inj ury in rats in vivo |
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| DOI： |
| 中文关键词: 舒芬太尼后处理 心肌缺血-再灌注损伤 PI3K/Akt |
| 英文关键词: Sufentanil postconditioning Myocardial ischemia-reperfusion injury Phos-phatidylinositol-3-kinase/protein-serine-threonine kinases |
| 基金项目:沈阳市科学技术项目计划(F13-221-9-71) |
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| 中文摘要: |
| 目的：探讨 PI3K/Akt 信号通路在舒芬太尼后处理减轻在体大鼠心肌缺血-再灌注损伤时细胞凋亡中的作用。方法取90只健康成年雄性 SD 大鼠,采用随机数字表法分为五组：假手术组(Sham 组),只穿线不结扎；缺血-再灌注组(IR 组),结扎左冠状动脉前降支造成心肌缺血30 min,再灌注120 min；舒芬太尼后处理组(Sufen 组),在灌注即刻,给予舒芬太尼1.0μg/kg 输注3min,再灌注处理同 IR 组；舒芬太尼后处理+LY294002(PI3K 抑制剂)组(SL 组),再灌注前10 min给予 LY2940020.3 mg/kg,并行舒芬太尼后处理；LY294002组(IL 组),再灌注前10 min 给予LY2940020.3 mg/kg,再灌注120 min。在缺血前即刻(T0)、缺血30 min(T1)、再灌注60 min(T2)和再灌注120 min(T3)时记录 HR 和 MAP；再灌注末,测定心肌梗死面积(IS/AAR)；再灌注15 min时,采用 Western blot 法测定心肌组织总的 Akt 和磷酸化的 Akt 蛋白含量；在再灌注末,用 RT-PCR检测 Bax 和 Bcl-2 mRNA 的表达。结果五组大鼠组间组内 HR 差异无统计学意义；T2、T3时 IR组、SL 组和 IL 组 MAP 明显低于 Sham 组(P <0.05)；Sufen 组 IS/AAR 明显低于 IR、SL 和 IL 组(P<0.05)；五组心肌总的 Akt 蛋白含量表达差异无统计学意义；与 Sufen 组比较,sham、IR、SL 和 IL组磷酸化的 Akt 表达明显下调(P <0.05),IR 组、SL 和 IL 组 Bax mRNA 的表达明显升高,Bcl-2 mRAN 的表达明显降低(P <0.05)。结论舒芬太尼后处理可减轻心肌缺血-再灌注损伤,可能与激活 PI3K/Akt 信号通路,降低 Bax 和增加 Bcl-2蛋白表达而达到抑制心肌细胞的凋亡有关。 |
| 英文摘要: |
| Objective To investigate the effect of sufentanil postconditioning on myocardial is-chemia-reperfusion injury in rats in vivo and the role of PI3K/Akt signaling pathway. Methods Ninety healthy male SD rats were randomly allocated to Sham group(the coronary suture was passed,not tied,and maintained for 1 50 min),group IR (ischemia for 30 min followed by 120 min reperfusion),group Sufen (administration of 1 μg/kg sufentanil for 3 min at the onset of reperfu-sion following 30 min of ischemia),group SL (administration of sufentanil and 0.3 mg/kg LY294002 DMSO)for 10 min prior to reperfusion)and group IL (only administration 0.3 mg/kg LY294002 for 10 min prior to reperfusion).HR and MAP were measured at the following time points:end of stabi-lization prior to ischemia (baseline);30 min of ischemia;60 and 120 min of reperfusion;at the end of 120 min reperfusion,the rats were sacrificed for assessment infarct area,the expression of Bax and Bcl-2 mRNA;the myocardial tissue samples were collected 1 5 min following reperfusion to determine the total and phosphorylated Akt expression by Western blot.Results There were no significant differences in the HR among the 6 groups;MAP were significantly decreased at 60 and 120 min fol-lowing reperfusion (P <0.05)in group IR,groups SL and IL compared to group Sham;there were no significant differences in the total Akt expression among the 6 groups;phosphorylated Akt were significantly upregulated,the infarct area were significantly decreased,Bax mRNA levels were signif-icantly decreased and Bcl-2 mRNA levels were significantly increased (P <0.05)in group Sufen com-pared to group IR,there were no significant differences respectively between groups SL,IL and IR. Conclusion Sufentanil postconditioning can induce myocardial protection through activation of the PI3K/Akt signaling pathway and inhibition of cell apoptosis via down-regulation Bax and up-regulation Bcl-2 expression. |
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