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首页> 外文期刊>American Journal of Physiology >PPARgamma activation, by reducing oxidative stress, increases NO bioavailability in coronary arterioles of mice with Type 2 diabetes.
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PPARgamma activation, by reducing oxidative stress, increases NO bioavailability in coronary arterioles of mice with Type 2 diabetes.

机译：通过降低氧化应激，PPARγ激活可增加2型糖尿病小鼠冠状小动脉中NO的生物利用度。

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We tested the hypothesis that short-term treatment of mice with Type 2 diabetes mellitus (DM) with rosiglitazone (ROSI), an agonist of peroxisome proliferator-activated receptor-gamma, ameliorates the impaired coronary arteriolar dilation by reducing oxidative stress via a mechanism unrelated to its effect on hyperglycemia and hyperinsulinemia. Control and Type 2 DM (db/db) mice were treated with ROSI (3 mg x kg(-1) x day(-1)) for 7 days, which did not significantly affect their serum concentration of glucose and insulin. Compared with controls, in db/db mice serum levels of 8-isoprostane and dihydroethydine-detectable superoxide production in carotid arteries were significantly elevated and were reduced by ROSI treatment. In coronary arterioles (diameter, approximately 80 microm) isolated from db/db mice, the reduced dilations to ACh, the nitric oxide (NO) donor NONOate, and increases in flow were significantly augmented either by in vitro administration of apocynin, an inhibitor of NAD(P)H-oxidase, or by in vivo ROSI treatment, responses that were then significantly reduced by the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester. In aortas of db/db mice, activity of SOD and catalase was reduced, whereas NAD(P)H oxidase activity was enhanced. ROSI treatment enhanced catalase and reduced NAD(P)H oxidase activity but did not affect the activity of SOD. These findings suggest that ROSI treatment enhances NO mediation of coronary arteriolar dilations due to the reduction of vascular NAD(P)H oxidase-derived superoxide production and enhancement of catalase activity. Thus, in addition to the previously revealed beneficial metabolic effects, the antioxidant action of rosiglitazone may protect coronary arteriolar function in Type 2 DM.
机译：我们测试了以下假设：用过氧化物酶体增殖物激活受体-γ的激动剂罗格列酮（ROSI）短期治疗2型糖尿病（DM）小鼠可通过不相关的机制降低氧化应激，从而减轻冠状动脉扩张的受损。其对高血糖和高胰岛素血症的作用。对照组和2型DM（db / db）小鼠用ROSI（3 mg x kg（-1）x day（-1））治疗7天，这不会显着影响其血清葡萄糖和胰岛素浓度。与对照组相比，在db / db小鼠中，颈动脉中的8-异前列腺素和二氢乙二胺可检测的超氧化物生成的血清水平显着升高，并且通过ROSI治疗而降低。从db / db小鼠中分离出的冠状小动脉（直径约80微米）中，通过体外给予Apocynin（一种抑制ACh的抑制剂），ACh的扩张减少，一氧化氮（NO）供体NONOate和血流的增加均显着增加。 NAD（P）H-氧化酶或通过体内ROSI处理，可通过NO合酶抑制剂N（ω）-硝基-L-精氨酸甲酯大大降低反应。在db / db小鼠的主动脉中，SOD和过氧化氢酶的活性降低，而NAD（P）H氧化酶的活性增强。 ROSI处理可增强过氧化氢酶并降低NAD（P）H氧化酶活性，但不影响SOD活性。这些发现表明，由于减少了血管NAD（P）H氧化酶衍生的超氧化物的产生并增强了过氧化氢酶的活性，ROSI治疗增强了NO介导的冠状动脉扩张。因此，除先前揭示的有益代谢作用外，罗格列酮的抗氧化作用还可以保护2型DM中的冠状动脉功能。

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