首页> 外文期刊>Diabetes, obesity & metabolism >NADPH oxidase inhibitor, apocynin, restores the impaired endothelial-dependent and -independent responses and scavenges superoxide anion in rats with type 2 diabetes complicated by NO dysfunction.
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NADPH oxidase inhibitor, apocynin, restores the impaired endothelial-dependent and -independent responses and scavenges superoxide anion in rats with type 2 diabetes complicated by NO dysfunction.

机译:NADPH氧化酶抑制剂Apocynin可恢复2型糖尿病并发NO功能异常的大鼠内皮依赖性和非依赖性应答受损,并清除超氧阴离子。

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Objective: We investigated the effect of apocynin, an NADPH oxidase inhibitor, in the impairment of vascular responses in Otsuka Long-Evans Tokushima Fatty (OLETF) rats (type 2 diabetic rat model) with or without (w/wo) N-nitro-l-arginine methyl ester treatment. Methods: Male OLETF and littermate Long-Evans Tokushima Otsuka (LETO) (28 weeks old) rats were separated as follows: LETO w/wo apocynin (Gp C, Gp C-apo), OLETF w/wo apocynin (Gp DM, Gp DM-apo) and OLETF plus l-nitro arginine acetate ester w/wo apocynin (Gp DMLN, Gp DMLN-apo). Five days after, peritoneal macrophages were stimulated with thioglycolate. Two days after, they were evaluated. Results: Plasma glucose and lipid levels remained unchanged. Acetylcholine-induced nitric oxide-dependent (NO-dependent) relaxation and nitroglycerin-induced NO-independent relaxation were improved in the Gp DMLN-apo, compared with that in Gp DMLN. Tone-related basal NO release and plasma NO(2) (-) and NO(3) (-) tended to be lower in Gp DM and Gp DMLN groups. The increased amount of superoxide anion released from macrophages in Gp DM and Gp DMLN was restored by apocynin. Intimal thickening was observed in aortae of Gp DM and Gp DMLN animals; however, there was little in aortae of Gp DM-apo and Gp DMLN(-) apo rats. Increased tumour necrosis factor-alpha (TNF-alpha) in the Gp DM and Gp DMLN was also restored by apocynin treatment. Conclusion: Apocynin restores the impairment of endothelial and non-endothelial function in diabetic angiopathy in OLETF without changing plasma glucose and lipid levels. NO and O(2) (-) may play a role in this process by decreasing TNF-alpha levels.
机译:目的:我们研究了NADPH氧化酶抑制剂Apocynin在有或没有(w / wo)N-硝基-的Otsuka Long-Evans Tokushima Fatty(OLETF)大鼠(2型糖尿病大鼠模型)中对血管反应损害的作用。 l-精氨酸甲酯处理。方法:雄性OLETF和同窝的长岛伊万德·德岛大冢(LETO)(28周龄)大鼠分离如下:LETO w / w ao accynin(Gp C,Gp C-apo),OLETF w / wo apocynin(Gp DM,Gp DM-apo)和OLETF加上1-硝基精氨酸乙酸酯w / w apocynin(Gp DMLN,Gp DMLN-apo)五天后,用巯基乙酸盐刺激腹膜巨噬细胞。两天后,他们进行了评估。结果:血浆葡萄糖和脂质水平保持不变。与Gp DMLN相比,Gp DMLN-apo改善了乙酰胆碱诱导的一氧化氮依赖性(NO依赖性)弛豫和硝酸甘油诱导的NO依赖性松弛。在Gp DM和Gp DMLN组中,与音有关的基础NO释放和血浆NO(2)(-)和NO(3)(-)趋于降低。载有Apocynin的蛋白可以恢复Gp DM和Gp DMLN中巨噬细胞释放的超氧化物阴离子的量增加。在Gp DM和Gp DMLN动物的主动脉中观察到内膜增厚。然而,Gp DM-apo和Gp DMLN(-)apo大鼠的主动脉中几乎没有。 Apocynin治疗还可以恢复Gp DM和Gp DMLN中增加的肿瘤坏死因子-α(TNF-α)。结论:Apocynin可以恢复OLETF糖尿病血管病的内皮和非内皮功能损伤,而无需改变血浆葡萄糖和脂质水平。 NO和O(2)(-)可能在此过程中通过降低TNF-alpha水平发挥作用。

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