Effects of pentoxifylline on oxidative stress and levels of EGF and NO in blood of diabetic type-2 patients; a randomized, double-blind placebo-controlled clinical trial

被引:73
作者
Radfar, M
Larijani, B
Hadjibabaie, M
Rajabipour, B
Mojtahedi, A
Abdollahi, M
机构
[1] Univ Tehran Med sci, Fac Pharm, Tehran, Iran
[2] Univ Tehran Med sci, Pharmaceut Sci Res Ctr, Tehran, Iran
[3] Univ Tehran Med sci, Sch Med, Tehran, Iran
[4] Univ Tehran Med sci, Endocrinol & Metab Res Ctr, Tehran, Iran
关键词
type-2 diabetes mellitus; oxidative stress; nitric oxide; epidermal growth factor; pentoxifylline;
D O I
10.1016/j.biopha.2005.05.003
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 [基础医学];
摘要
Background. - As oxidative stress contributes to both progression and pathologic complications of diabetes and effective therapeutic strategies to prevent or delay the damage remain limited, the aim of the present study was to assess the efficacy of pentoxifylline in reducing of oxidative stress. Since there is a relationship between nitric oxide (NO), epidermal growth factor (EGF) and oxidative stress, we measured the effect of this drug on these parameters in comparison to placebo. Methods. - Thirty-nine patients with type-2 diabetes mellitus were randomized in a double blind, placebo-controlled clinical trial to receive either pentoxifylline 400 mg four times a day or placebo for 14 days. Blood samples were obtained at baseline and at the end of the study. Samples were analyzed for thiobarbituric reactive substances (TBARS) as a marker of lipid peroxidation, ferric reducing ability (total antioxidant power, TAP), EGF and NO levels. Results. - Pentoxifylline in comparison to placebo was effective (P < 0.05) in reduction of lipid peroxidation in plasma of the patients without significant effects on TAP, levels of EGF and NO in plasma. Conclusion. - Adding of pentoxifylline to drug regimen of diabetic type-2 patients can be helpful. Exact mechanism of action of pentoxifylline in reduction of blood lipid peroxidation remains to be elucidated. (c) 2005 Elsevier SAS. All rights reserved.
引用
收藏
页码:302 / 306
页数:5
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