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在四氧嘧啶诱导的糖尿病大鼠模型中,氧化应激与血管功能障碍无关。

Oxidative stress is not associated with vascular dysfunction in a model of alloxan-induced diabetic rats.

作者信息

Capellini Verena Kise, Baldo Caroline Floreoto, Celotto Andréa Carla, Batalhão Marcelo Eduardo, Cárnio Evelin Capellari, Rodrigues Alfredo José, Evora Paulo Roberto Barbosa

机构信息

Departamento de Cirurgia e Anatomia, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.

出版信息

Arq Bras Endocrinol Metabol. 2010 Aug;54(6):530-9. doi: 10.1590/s0004-27302010000600004.

DOI:10.1590/s0004-27302010000600004
PMID:20857057
Abstract

OBJECTIVES

To verify if an experimental model of alloxan-diabetic rats promotes oxidative stress, reduces nitric oxide bioavailability and causes vascular dysfunction, and to evaluate the effect of N-acetylcysteine (NAC) on these parameters.

METHODS

Alloxan-diabetic rats were treated or not with NAC for four weeks. Plasmatic levels of malondialdehyde (MDA) and nitrite/nitrate (NOx), the endothelial and inducible nitric oxide synthase (eNOS and iNOS) immunostaining and the vascular reactivity of aorta were compared among diabetic (D), treated diabetic (TD) and control (C) rats.

RESULTS

MDA levels increased in D and TD. NOx levels did not differ among groups. Endothelial eNOS immunostaining reduced and adventitial iNOS increased in D and TD. The responsiveness of rings to acetylcholine, sodium nitroprusside, and phenylephrine did not differ among groups.

CONCLUSIONS

NAC had no effect on the evaluated parameters and this experimental model did not promote vascular dysfunction despite the development of oxidative stress.

摘要

目的

验证四氧嘧啶糖尿病大鼠实验模型是否会促进氧化应激、降低一氧化氮生物利用度并导致血管功能障碍,并评估N-乙酰半胱氨酸(NAC)对这些参数的影响。

方法

四氧嘧啶糖尿病大鼠接受或不接受NAC治疗四周。比较糖尿病(D)组、接受治疗的糖尿病(TD)组和对照组(C)大鼠的血浆丙二醛(MDA)和亚硝酸盐/硝酸盐(NOx)水平、内皮型和诱导型一氧化氮合酶(eNOS和iNOS)免疫染色以及主动脉的血管反应性。

结果

D组和TD组的MDA水平升高。各组之间NOx水平无差异。D组和TD组的内皮eNOS免疫染色减少,外膜iNOS增加。各组血管环对乙酰胆碱、硝普钠和去氧肾上腺素的反应性无差异。

结论

NAC对所评估的参数没有影响,并且尽管发生了氧化应激,但该实验模型并未促进血管功能障碍。

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