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α-硫辛酸治疗改善了糖尿病大鼠主动脉的内皮依赖性舒张功能。

Alpha lipoic acid treatment improved endothelium-dependent relaxation in diabetic rat aorta.

作者信息

Okudan N, Nurullahoğlu Atalik K E, Gökbel H, Canbilen A, Kara I

机构信息

Department of Physiology, Meram Faculty of Medicine, Selçuk University, Konya, Turkey.

出版信息

Yakugaku Zasshi. 2011;131(5):739-44. doi: 10.1248/yakushi.131.739.

DOI:10.1248/yakushi.131.739
PMID:21532270
Abstract

The aim of this study was to ascertain the effects of α-lipoic acid (ALA) treatment on relaxant responses of acetylcholine (ACh) and isoprenaline (ISO) in aortic rings precontracted with serotonin (5-HT, 10(-6) M) obtained from streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in the rats by 50 mg/kg streptozotocin (STZ) via an intraperitoneal injection. Rat body and aorta weights were measured. The isometric tension to ACh (10(-9)-3×10(-6) M) and ISO (10(-9)-10(-4) M) of 5-HT-precontracted diabetic and non-diabetic rat (control), diabetic-ALA-treated, and ALA-treated aortas, in organ baths were recorded. Six weeks after STZ treatment blood glucose was elevated compared to control rats. In aortic rings from diabetic rats ACh and ISO-induced relaxations were impaired whereas endothelium-independent relaxation to sodium nitroprusside (SNP) was unaffected. ALA (100 mg/kg/day) treatment for 5 weeks enhanced ACh and ISO-induced relaxation in diabetic aortas. This recovering effect was via NO because prevented by incubating the vessels with N(G)-nitro-L-arginine methyl ester (L-NAME, a NOS inhibitor). It may be assumed that ALA treatment in vivo, can protect against impaired vascular responsiveness in STZ-induced diabetic rats.

摘要

本研究旨在确定α-硫辛酸(ALA)处理对从链脲佐菌素(STZ)诱导的糖尿病大鼠获得的、用5-羟色胺(5-HT,10⁻⁶ M)预收缩的主动脉环中乙酰胆碱(ACh)和异丙肾上腺素(ISO)舒张反应的影响。通过腹腔注射50 mg/kg链脲佐菌素(STZ)诱导大鼠患糖尿病。测量大鼠的体重和主动脉重量。记录在器官浴中5-HT预收缩的糖尿病和非糖尿病大鼠(对照)、糖尿病-ALA处理组和ALA处理组主动脉对ACh(10⁻⁹ - 3×10⁻⁶ M)和ISO(10⁻⁹ - 10⁻⁴ M)的等长张力。STZ处理六周后,与对照大鼠相比血糖升高。在糖尿病大鼠的主动脉环中,ACh和ISO诱导的舒张受损,而对硝普钠(SNP)的非内皮依赖性舒张未受影响。ALA(100 mg/kg/天)处理5周增强了糖尿病主动脉中ACh和ISO诱导的舒张。这种恢复作用是通过一氧化氮(NO)实现的,因为用N⁰-硝基-L-精氨酸甲酯(L-NAME,一种一氧化氮合酶抑制剂)孵育血管可阻止这种作用。可以推测,体内ALA处理可预防STZ诱导的糖尿病大鼠血管反应性受损。

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