基础医学与临床 ›› 2018, Vol. 38 ›› Issue (8): 1064-1068.

• 研究论文 • 上一篇    下一篇

脂联素抑制高浓度胰岛素诱导的大鼠心肌细胞肥大

轩辕东1,刘雅娟2,任永康3,徐璐3,朱娜1,杨锐英2   

  1. 1. 宁夏医科大学
    2. 宁夏医科大学总医院
    3. 宁夏医科大学雁湖校区
  • 收稿日期:2017-11-06 修回日期:2018-05-02 出版日期:2018-08-05 发布日期:2018-07-24
  • 通讯作者: 杨锐英 E-mail:yangruiying@medmail.com.cn
  • 基金资助:
    脂联素与心室重构

Adiponectin inhibits cardiomyocyte hypertrophy induced by high concentration of insulin in rats

  • Received:2017-11-06 Revised:2018-05-02 Online:2018-08-05 Published:2018-07-24

摘要: 目的 探讨脂联素(APN)是否通过上调AdipoR1/AMPK/PI3K/AKT抑制高浓度胰岛素诱导的大鼠心肌细胞肥大。方法 分离新生SD大鼠心肌细胞并连续培养9 d,按干预条件不同将心肌细胞分为4组:对照组(培养基)、模型组(1×10-6mol/L胰岛素)、干预组(1×10-6mol/L胰岛素+7.5mg/L脂联素)和转染组(AdipoR1 siRNA 转染后胰岛素+脂联素处理)。48 h后检测各组心肌细胞的平均蛋白含量、3-甲基组氨酸(3-MH)含量及心肌细胞表面积;Western blot检测脂联素受体1(AdipoR1)、腺苷酸活化蛋白激酶(AMPK)、磷脂酰肌醇3-激酶(PI3K)和蛋白激酶B(AKT)蛋白的表达。结果 与对照组相比,模型组心肌细胞平均蛋白含量增多(P<0.05,n=3)、3-MH含量减少(P<0.05,n=3)及心肌细胞相对表面积增大(P<0.01,n=10);与模型组相比,干预组上述变化显著减轻,干预组AdipoR1、AMPK、PI3K和AKT蛋白表达量增加(P<0.05,n=3)。结论 脂联素可通过上调AdipoR1/AMPK/PI3K/AKT抑制高浓度胰岛素诱导的大鼠心肌细胞肥大。

关键词: 心力衰竭, 心肌细胞肥大, 脂联素, AMPK, PI3K/AKT

Abstract: Objective To investigate whether adiponectin (APN) inhibits cardiomyocyte hypertrophy induced by high concentration of insulin by up-regulating AdipoR1 / AMPK / PI3K / AKT. Methods The cardiomyocytes of neonatal SD rats were isolated and cultured continuously for 9 days. Cardiomyocytes were divided into 4 groups according to different intervention conditions: control group (medium), model group (1×10-6 mol/L insulin), intervention group (1×10-6 mol/L insulin+7.5 mg/L adiponectin) and transfection group (AdipoR1 siRNA insulin + adiponectin processing after transfection). After 48 h, the average protein content, 3-methylhistidine (3-MH) content and myocardial cell surface area of each group were detected. Western blot was used to detect the expression of AdipoR1, AMPK, PI3K and AKT proteins. Results Compared with the control group, the average protein content of myocardial cells increased (P<0.05, n=3), the content of 3-MH decreased (P<0.05, n=10). Compared with the model group, the above changes in the intervention group were significantly reduced, while the expression of AdipoR1, AMPK, PI3K and AKT in the intervention group was increased (P<0.05, n=3) . Conclusion Adiponectin may inhibit rat cardiomyocyte hypertrophy induced by high concentration of insulin by up-regulating AdipoR1 / AMPK / PI3K / AKT.

Key words: heart failure, Myocyte hypertrophy, Adiponectin, AMPK, PI3K/AKT