本文關(guān)鍵詞：運(yùn)動(dòng)和羅格列酮降低ADMA的協(xié)同作用及其機(jī)制研究　出處：《中國(guó)體育科技》2016年06期 　論文類(lèi)型：期刊論文

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【摘要】：目的:研究運(yùn)動(dòng)與羅格列酮聯(lián)合對(duì)T2DM大鼠ADMA水平的影響,觀察其是否存在協(xié)同效應(yīng)。方法:采用高質(zhì)飲食結(jié)合腹腔注射低劑量STZ的方法建立T2DM大鼠模型,將實(shí)驗(yàn)動(dòng)物分為正常對(duì)照組、T2DM組、T2DM+運(yùn)動(dòng)組、T2DM+羅格列酮組和T2DM+運(yùn)動(dòng)+羅格列酮組,每組給予相應(yīng)的干預(yù)10周。結(jié)果:羅格列酮可以降低T2DM大鼠CML(P0.01)和ADMA(P0.01),同時(shí)上調(diào)肝臟PPAR-γ(P0.01)和DDAH-1(P0.01)mRNA表達(dá),而運(yùn)動(dòng)可以降低T2DM大鼠CML(P0.01)和ADMA(P0.05),同時(shí)上調(diào)肝臟PPAR-γ(P0.05)和DDAH-1(P0.01)mRNA表達(dá);運(yùn)動(dòng)和羅格列酮聯(lián)合干預(yù)組CML明顯低于羅格列酮單獨(dú)干預(yù)(P0.01),ADMA明顯低于單獨(dú)運(yùn)動(dòng)干預(yù)(P0.05),肝臟PPAR-γ和DDAH-1mRNA表達(dá)分別顯著高于單獨(dú)運(yùn)動(dòng)((P0.01)和單獨(dú)羅格列酮(P0.01)干預(yù)。結(jié)論:運(yùn)動(dòng)和羅格列酮在降低ADMA保護(hù)血管內(nèi)皮方面可能存在協(xié)同效應(yīng),其機(jī)制可能是基于AGEs/PPAR-γ/DDAH/ADMA途徑。
[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- 緯 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- 緯 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- 緯 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- 緯 -DDAH / ADMA pathway.
【作者單位】： 中國(guó)藥科大學(xué);東南大學(xué)醫(yī)學(xué)院;
【基金】：中央高�？蒲谢�(ZJ13076)
【分類(lèi)號(hào)】：R587.1
【正文快照】： 血管內(nèi)皮功能異常被認(rèn)為是糖尿病大血管并發(fā)癥和糖尿病微血管病變的共同病理生理特征,目前研究[20]發(fā)現(xiàn),一氧化氮(Nitric Oxide,NO)生物利用度降低導(dǎo)致的內(nèi)皮功能受損在糖尿病血管并發(fā)癥的發(fā)生發(fā)展中起重要作用,而導(dǎo)致NO生物利用度降低的主要原因是高血糖引發(fā)的氧化應(yīng)激增加。，

本文編號(hào)：1416111