上海交通大学学报（医学版）

上海交通大学学报（医学版）

• 论著（基础研究） • 上一篇    下一篇

妊娠期糖尿病对大鼠雌性子代缺血再灌注后心脏收缩功能的影响及其机制

邹虹1，姜小雪2，王寒冰1，袁雨1，罗晓芳1，谭彬1，张华1，Philip N Baker1,3，童超1，漆洪波1   

  1. 1.重庆医科大学附属第一医院妇产科 中国-加拿大-新西兰联合母胎医学实验室，重庆 400016； 2.重庆医科大学附属第一医院心内科， 重庆 400016; 3.奥克兰大学Liggins研究所， 奥克兰 1142， 新西兰
  • 出版日期:2016-02-28 发布日期:2016-03-29
  • 通讯作者: 漆洪波, 电子信箱: qihongbo@sina.com; 童超, 电子信箱: chaotongcqmu@163.com。
  • 作者简介:邹虹（1989—）， 女， 住院医师， 硕士; 电子信箱: ayzouhong@163.com。

Effects of gestational diabetes mellitus on cardiac contractile function of female offspring rats after ischemia/reperfusion and underlying mechanisms

ZOU Hong1, JIANG Xiao-xue2, WANG Han-bing1, YUAN Yu1, LUO Xiao-fang1, TAN Bing1, ZHANG Hua1, Philip N Baker1,3, TONG Chao1,2, QI Hong-bo1   

  1. 1.Department of Gynaecology and Obstetrics, China-Canada-New Zealand Joint Laboratory of Maternal and Fetal Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China; 2.Department of Cardiology, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China； 3.the Liggins Institute, University of Auckland, Auckland 1142, New Zealand
  • Online:2016-02-28 Published:2016-03-29

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摘要：

目的 利用大鼠模型探讨妊娠期糖尿病(GDM)对雌性子代心脏功能的影响及潜在机制。方法 雌性野生型SD大鼠在妊娠中期给予腹腔注射链脲佐菌素（35 mg/kg）建立GDM模型（GDM组），另设正常对照组。分娩后，雌性F1子代饲养至24周，期间测定随机血糖、血压和心率，进行葡萄糖耐量试验、胰岛素耐量试验。构建心脏离体缺血再灌注（I/R）模型，Western blotting检测心脏蛋白激酶B (Akt)、腺苷酸激活蛋白激酶(AMPK)和乙酰辅酶A羧化酶(ACC)信号通路。结果 GDM组雌性F1子代离体I/R后心脏收缩功能显著低于正常对照组（P=0.048 6）；Western blotting显示离体I/R后GDM组雌性F1子代大鼠心脏AMPK和ACC磷酸化水平显著低于正常对照组（P=0.005 6）。结论 GDM可引起子代雌性大鼠对心脏I/R损伤不耐受，这可能与其心脏AMPK磷酸化对I/R刺激反应迟钝有关。

关键词: 妊娠期糖尿病, 子代, 心脏缺血再灌注

Abstract:

Objective To investigate the effects of gestational diabetes mellitus (GDM) on the cardiac function of female offspring rats and underlying mechanisms by the rat model. Methods Wild type female SD rats were injected with streptozotocin (35 mg/kg) in the second trimester of pregnancy to establish the GDM model (GDM group). The control group was also established. Female F1 offspring rats were fed for 24 weeks after they were born. During this period, random blood glucose level, blood pressure, and heart rate were measured and glucose tolerance test and insulin tolerance test were conducted. The in vitro myocardial ischemia/reperfusion (I/R) model was established. The signaling pathways of protein kinase B (Akt), adenine monophosphate activated protein kinase (AMPK), and acetyl-coenzyme A carboxylase (ACC) in cardiac tissues were detected by Western blotting. Results The in vitro cardiac contractile function of female F1 offspring of the GDM group after I/R was significantly weaker than that of the control group (P=0.048 6). The results of Western blotting showed that the phosphorylation of AMPK and ACC in cardiac tissues of female F1 offspring of the GDM group after in vitro I/R was significantly lower than that of the control group (P=0.005 6). Conclusion GDM results in cardiac I/R intolerance of female offspring rats, which may be relevant to the blunt response to I/R stimulation caused by the phosphorylation of AMPK.

Key words: gestational diabetes mellitus, offspring, cardiac ischemia and reperfusion