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脂联素后处理对大鼠心肌缺血/再灌注损伤的影响及ADP/PI3K/Akt信号通路的作用
引用本文:赵林静,崔柳苏,张金盈,王永玲. 脂联素后处理对大鼠心肌缺血/再灌注损伤的影响及ADP/PI3K/Akt信号通路的作用[J]. 中国应用生理学杂志, 2017, 33(4): 308-313. DOI: 10.12047/j.cjap.5531.2017.075
作者姓名:赵林静  崔柳苏  张金盈  王永玲
作者单位:1. 新乡医学院基础医学院, 河南 新乡 453003;2. 郑州大学第一附属医院心血管内科, 河南 郑州 450000
基金项目:新乡医学院博士科研启动基金资助(XYBSKYZZ 201634)
摘    要:目的:探讨脂联素(ADP)后处理对大鼠心肌缺血/再灌注损伤(MIRI)的影响以及脂联素/磷脂酰肌醇-3激酶/蛋白激酶B (ADP/PI3K/Akt)通路的作用。方法:SD大鼠麻醉后气管插管连接呼吸机,开胸暴露心肌,在左心耳和肺动脉圆锥之间用带线圆针对冠脉左前降支(LAD)穿线,LAD结扎断流30 min后松线再灌注120 min,建立大鼠MIRI模型。大鼠随机分为以下5组(n=12):①假手术组(Sham组):LAD仅穿线不结扎;② MIRI组;③ADP后处理组(ADP组):LAD断流10 min时静注ADP继续断流20 min,然后再灌注120 min;④ADP+LY294002组:LAD断流10 min时静注ADP和LY294002,其余同ADP组;⑤LY294002组:LAD断流10 min时静注LY294002,其余同ADP组。各组取血检测LDH和cTnI含量,取左心室心肌测定PI3k、Akt、p-Akt、ADPmRNA、ADPR1mRNA和PI3KmRNA表达。结果:与Sham组比较,MIRI组血浆LDH和cTnI均明显升高(P<0.05);和MIRI组相比,ADP组心肌损伤指标明显下降(P<0.05),而应用LY294002的两组心肌损伤比ADP组加重(P<0.05)。ADP组心肌PI3K、p-Akt、ADPmRNA、ADPR1mRNA和PI3kmRNA表达比MIRI组升高(P<0.05),应用LY294002两组上述5个指标比MIRI组降低(P<0.05)。结论:ADP后处理对大鼠MIRI有保护作用,ADP/PI3K/Akt通路参与了以上作用。

关 键 词:脂联素  缺血后处理  心肌缺血/再灌注损伤  信号转导通路  磷脂酰肌醇-3激酶  磷酸化的蛋白激酶B  大鼠  
收稿时间:2016-11-28

Effect of adiponectin postconditioning against myocardial ischemia/reperfusion injury in rats and role of ADP/PI3K/Akt pathway in adiponectin postconditioning
ZHAO Lin-jing,CUI Liu-su,ZHANG Jin-ying,WANG Yong-ling. Effect of adiponectin postconditioning against myocardial ischemia/reperfusion injury in rats and role of ADP/PI3K/Akt pathway in adiponectin postconditioning[J]. Chinese journal of applied physiology, 2017, 33(4): 308-313. DOI: 10.12047/j.cjap.5531.2017.075
Authors:ZHAO Lin-jing  CUI Liu-su  ZHANG Jin-ying  WANG Yong-ling
Affiliation:1. School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003;2. Department of Vasculocardiology, First Affiliated Hospital, Zhengzhou University, Zhengzhou 450000, China
Abstract:Objective: To investigate the effects of adiponectin(ADP) postconditioning against myocardial ischemia/reperfusion injury(MIRI) in rats and role of ADP/PI3K/Akt pathway in ADP postconditioning.Methods: SD rat was connected to ventilator by tracheal intubation under anesthesia, then left anterior descending coronary artery (LAD) was threaded between left auricle and pulmonary artery cone after exposing heart by surgery. MIRI model was induced by ligation of LAD for 30 min and the following reperfusion for 120 min. Rats were divided randomly into 5 groups (n=12):① Sham group:LAD was threaded without ligation; ② MIRI group; ③ADP group (ADP postconditioning) were subjected to intravenous injection of ADP when LAD ligation for 10 min and the ligation held for 20 min after that, then reperfusion for 120 min; ④ ADP+LY294002 group were subjected to injection of ADP and LY294002 when LAD ligation for 10 min, the other steps were the same as ADP group; ⑤ LY294002 group were subjected to injection of LY294002 when LAD ligation for 10 min, the other steps were the same as ADP group. Titers of lactate dehydrogenase(LDH) and cardiac troponin I(cTnI) in plasma were observed, expressions of PI3K, Akt, phosphorylated-Akt(p-Akt), ADP mRNA, ADPR1 mRNA and PI3k mRNA in myocardial tissue were measured.Results: Compared with sham group, the levels of LDH and cTnI in MIRI group were increased (P<0.05); Compared with MIRI group, the levels of LDH and cTnI in ADP group were decreased (P<0.05); Compared with ADP group, the levels of LDH and cTnI were increased in LY294002 applying groups(P<0.05). Compared with MIRI group, the expressions of PI3K, p-Akt, ADP mRNA, ADPR1 mRNA and PI3K mRNA were increased in ADP group (P<0.05), the above mentioned 5 parameters in LY294002 applying groups were decreased(P<0.05).Conclusion: ADP postconditioning could reduce MIRI in rats, the protective effect might have relation to ADP/PI3k/Akt pathway.
Keywords:adiponectin  ischemic postconditioning  myocardial ischemia/reperfusion injury  signalling pathway  PI3K  p-Akt  rat  
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