在子宫内暴露于孕产妇糖尿病会通过激活循环氧化酶2-衍生性前列腺素来加剧饮食中摄入引起的内皮功能障碍
Rafael M Costa1,2,3,4, Débora Malta Cerqueira1,5, Lydia Francis1,5
1Department of Pediatrics, UPMC Children's Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, Pennsylvania, United States.
概括
产前暴露于母亲糖尿病,使后代在成年时因高盐饮食引起的血管功能障碍和炎症. 这通过氧化应激和前列腺素E2 (PGE2) 生成发生,突出显示母亲糖尿病是心血管风险因素.
科学领域:
- 心血管科学 心血管科学
- 内分泌学 在内分泌学.
- 发展生物学 发展生物学
背景情况:
- 母亲糖尿病是众所周知的后代心血管风险因素.
- 在高盐条件下,产前糖尿病暴露对血管健康的影响尚不清楚.
研究的目的:
- 调查是否在子宫内暴露于孕产妇糖尿病使后代易患高盐诱导的血管功能障碍.
- 阐明涉及氧化应激和前列腺路的潜在机制.
主要方法:
- 使用了一种与产前暴露于母体1型糖尿病的小鼠模型 (Ins2秋田小鼠).
- 成人后代 (DM_Exp) 接受了高盐饮食,并评估了血管功能 (电线肌图,乙胆诱导的放松),氧化应激 (过氧化) 和炎症标志物 (细胞因子,化学因子).
- 通过ELISA,qPCR和免疫化学分析了循环氧化酶 (COX) 路径组件 (COX2,PGE2);测试了抗氧化剂和COX抑制剂的作用.
主要成果:
- 暴露于母体糖尿病的后代在正常饮食中没有表现出血管功能障碍,但在高盐饮食中出现了内皮功能障碍和大动脉收缩性增加.
- 高盐饮食诱导了血管氧化应激,COX2表达,以及暴露后代的前列腺素E2 (PGE2) 过度产生的后代.
- 抗氧化剂 (tempol) 和COX抑制剂 (indomethacin,NS398) 改善了高盐诱导的内皮功能障碍.
- 暴露后代表现出循环中细胞因子和化学因子的增加,这表明血管炎症.
结论:
- 产前暴露于母体糖尿病会在成年后代中产生高盐诱导的血管功能障碍和炎症的倾向.
- 这种倾向是由增加的氧化应激和产生COX2-衍生PGE2.2的介导的.
- 怀孕期间产妇糖尿病被证实是成人心血管健康的重要风险因素.
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