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运动和罗格列酮降低ADMA的协同作用及其机制研究

发布时间:2018-01-12 21:32

  本文关键词:运动和罗格列酮降低ADMA的协同作用及其机制研究 出处:《中国体育科技》2016年06期  论文类型:期刊论文


  更多相关文章: 运动 罗格列酮 协同作用 ADMA DDAH- PPAR-γ


【摘要】:目的:研究运动与罗格列酮联合对T2DM大鼠ADMA水平的影响,观察其是否存在协同效应。方法:采用高质饮食结合腹腔注射低剂量STZ的方法建立T2DM大鼠模型,将实验动物分为正常对照组、T2DM组、T2DM+运动组、T2DM+罗格列酮组和T2DM+运动+罗格列酮组,每组给予相应的干预10周。结果:罗格列酮可以降低T2DM大鼠CML(P0.01)和ADMA(P0.01),同时上调肝脏PPAR-γ(P0.01)和DDAH-1(P0.01)mRNA表达,而运动可以降低T2DM大鼠CML(P0.01)和ADMA(P0.05),同时上调肝脏PPAR-γ(P0.05)和DDAH-1(P0.01)mRNA表达;运动和罗格列酮联合干预组CML明显低于罗格列酮单独干预(P0.01),ADMA明显低于单独运动干预(P0.05),肝脏PPAR-γ和DDAH-1mRNA表达分别显著高于单独运动((P0.01)和单独罗格列酮(P0.01)干预。结论:运动和罗格列酮在降低ADMA保护血管内皮方面可能存在协同效应,其机制可能是基于AGEs/PPAR-γ/DDAH/ADMA途径。
[Abstract]:Objective: to study the effect of exercise combined with rosiglitazone on ADMA level in T2DM rats. Methods: T2DM rat model was established by high quality diet and intraperitoneal injection of low dose STZ, and the experimental animals were divided into normal control group and T2DM group. Rosiglitazone group in T2DM exercise group and rosiglitazone group in T2DM exercise group. Results: rosiglitazone could reduce CML P0.01 and ADMAP 0.01) in T2DM rats. At the same time, the expression of PPAR- 纬 P0.01) and DDAH-1(P0.01)mRNA were upregulated. However, exercise could decrease the levels of CML P0.01 and ADMA-P0.05 in T2DM rats. At the same time, the expression of PPAR- 纬 P0.05) and DDAH-1(P0.01)mRNA were upregulated. CML in combined exercise and rosiglitazone intervention group was significantly lower than that in rosiglitazone alone intervention group (P0.05). The expression of PPAR- 纬 and DDAH-1mRNA in liver was significantly higher than that of P0.01) and rosiglitazone alone (P0.01). Conclusion: exercise and rosiglitazone may have synergistic effects on the protection of vascular endothelium from ADMA. The mechanism may be based on the ages / PPAR- 纬 -DDAH / ADMA pathway.
【作者单位】: 中国药科大学;东南大学医学院;
【基金】:中央高校科研基金(ZJ13076)
【分类号】:R587.1
【正文快照】: 血管内皮功能异常被认为是糖尿病大血管并发症和糖尿病微血管病变的共同病理生理特征,目前研究[20]发现,一氧化氮(Nitric Oxide,NO)生物利用度降低导致的内皮功能受损在糖尿病血管并发症的发生发展中起重要作用,而导致NO生物利用度降低的主要原因是高血糖引发的氧化应激增加。

本文编号:1416111

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