التفاصيل البيبلوغرافية
| العنوان: |
Role of oxidative stress-induced systemic and cavernosal molecular alterations in the progression of diabetic erectile dysfunction在糖尿病性勃起功能障碍的进展过程中氧化应激所诱导的全身以及海绵体分子变化的影响 |
| المؤلفون: |
Castela, Angela1,2, Gomes, Pedro1,3, Domingues, Valentina F.4, Paíga, Paula4, Costa, Raquel1, Vendeira, Pedro5, Costa, Carla1 |
| المصدر: |
Journal of Diabetes. May2015, Vol. 7 Issue 3, p393-401. 9p. |
| مصطلحات موضوعية: |
*IMPOTENCE, *DIABETES complications, *OXIDATIVE stress, *GLUTATHIONE, *IMMUNOHISTOCHEMISTRY |
| الملخص (بالإنجليزية): |
Background Erectile dysfunction ( ED) is a prevalent complication of diabetes, and oxidative stress is an important feature of diabetic ED. Oxidative stress-induced damage plays a pivotal role in the development of tissue alterations. However, the deleterious effects of oxidative stress in the corpus cavernosum with the progression of diabetes remain unclear. The aim of this study was to evaluate systemic and penile oxidative stress status in the early and late stages of diabetes. Methods Male Wistar streptozotocin-diabetic rats (and age-matched controls) were examined 2 (early) and 8 weeks (late) after the induction of diabetes. Systemic oxidative stress was evaluated by urinary H2O2 and the ratio of circulating reduced/oxidized glutathione ( GSH/GSSG). Penile oxidative status was assessed by H2O2 production and 3-nitrotyrosine (3- NT) formation. Cavernosal endothelial nitric oxide synthase ( eNOS) was analyzed by quantitative immunohistochemistry. Dual immunofluorescence was also performed for 3- NT and α-smooth muscle actin ( α- SMA) and eNOS- α- SMA. Results There was a significant increase in urinary H2O2 levels in both diabetic groups. The plasma GSH/GSSG ratio was significantly augmented in late diabetes. In cavernosal tissue, H2O2 production was significantly increased in late diabetes. Reactivity for 3- NT was located predominantly in cavernosal smooth muscle ( SM) and was significantly reduced in late diabetes. Quantitative immunohistochemistry revealed a significant decrease in eNOS levels in cavernosal SM and endothelium in late diabetes. Conclusions The findings indicate that the noxious effects of oxidative stress are more prominent in late diabetes. Increased penile protein oxidative modifications and decreased eNOS expression may be responsible for structural and/or functional deregulation, contributing to the progression of diabetes-associated ED. [ABSTRACT FROM AUTHOR] |
| Abstract (Chinese): |
摘要 背景：勃起功能障碍（Erectile dysfunction，ED）是一个普遍存在的糖尿病并发症，而氧化应激是糖尿病性ED的一个重要特征。氧化应激所诱导的损害在组织变化的进展中起着举足轻重的作用。然而，随着糖尿病的进展，氧化应激对海绵体造成的有害影响目前仍未明确。这项研究的目的是在早期与晚期糖尿病患者中评估全身以及阴茎的氧化应激状态。 方法：雄性链脲霉素-糖尿病大鼠（以及鼠龄相匹配的对照组大鼠）在诱导出糖尿病后的第2周（早期）以及第8周（晚期）时接受测定。通过尿H2O2以及循环中的还原型/氧化型谷胱甘肽比值（GSH/GSSG）来评估全身的氧化应激情况。通过生成的H2O2以及形成的3-硝基酪氨酸（3-nitrotyrosine，3-NT）来评估阴茎的氧化应激情况。使用定量的免疫组织化学方法来分析海绵体内皮中的一氧化氮合成酶（nitric oxide synthase，eNOS）。使用双重免疫荧光法分析3-NT、 α-平滑肌肌动蛋白（ α-smooth muscle actin， α-SMA）以及eNOS- α-SMA。 结果：在两个糖尿病组中尿H2O2水平均显著升高。晚期糖尿病组血浆中的GSH/GSSG比值显著增加。在海绵体组织中，晚期糖尿病组生成的H2O2显著增加。对3-NT的反应主要位于海绵体平滑肌，在晚期糖尿病组显著下降。定量免疫组织化学分析结果显示，晚期糖尿病组海绵体平滑肌以及内皮组织中的eNOS水平显著下降。 结论：研究结果提示在晚期糖尿病组中氧化应激造成的有害影响更为显著。阴茎中的蛋白氧化修饰增加以及eNOS表达减少可能是结构和/或功能异常的原因，结果导致了糖尿病性ED的进展。 [ABSTRACT FROM AUTHOR] |
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