黑草对链脲佐菌素诱导的糖尿病大鼠氧化应激和β细胞损伤的影响。

Mehmet Kanter, Omer Coskun, Ahmet Korkmaz, Sukru Oter
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引用次数: 203

摘要

本研究旨在探讨黑草(Nigella sativa L., NS)对链脲佐菌素(STZ)诱导的糖尿病大鼠β细胞损伤的保护作用。STZ单次腹腔注射50 mg/kg诱导糖尿病。在STZ给药前3天注射NS (0.2 ml/kg/天,i.p.),并在整个4周的研究中持续注射。氧化应激被认为在糖尿病(DM)的发病机制中起作用。为了评估细胞抗氧化防御系统的变化,我们测量了胰腺匀浆中抗氧化酶(如谷胱甘肽过氧化物酶(GSHPx)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT))的活性。我们还测量了血清一氧化氮(NO)、红细胞和胰腺组织丙二醛(MDA)水平(脂质过氧化的标志物),以确定氧化和抗氧化状态之间是否存在不平衡。免疫组化法检测胰腺β细胞。STZ诱导小鼠脂质过氧化和血清NO浓度显著升高,抗氧化酶活性显著降低。NS处理通过降低脂质过氧化和血清NO,增加抗氧化酶活性来提供保护作用。糖尿病大鼠胰岛细胞变性,胰岛素免疫组化染色减弱。胰岛素染色强度的增加和β细胞数量的保存在ns治疗的糖尿病大鼠中是明显的。这些发现表明,NS治疗通过降低氧化应激和保持胰腺β细胞完整性对糖尿病具有治疗保护作用。因此,NS可能在临床上对保护β细胞免受氧化应激有帮助。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of Nigella sativa on oxidative stress and beta-cell damage in streptozotocin-induced diabetic rats.

The aim of the present study was to evaluate the possible protective effects of Nigella sativa L. (NS) against beta-cell damage from streptozotocin (STZ)-induced diabetes in rats. STZ was injected intraperitoneally at a single dose of 50 mg/kg to induce diabetes. NS (0.2 ml/kg/day, i.p.) was injected for 3 days prior to STZ administration, and these injections were continued throughout the 4-week study. Oxidative stress is believed to play a role in the pathogenesis of diabetes mellitus (DM). To assess changes in the cellular antioxidant defense system, we measured the activities of antioxidant enzymes (such as glutathione peroxidase (GSHPx), superoxide dismutase (SOD), and catalase (CAT)) in pancreatic homogenates. We also measured serum nitric oxide (NO) and erythrocyte and pancreatic tissue malondialdehyde (MDA) levels, a marker of lipid peroxidation, to determine whether there is an imbalance between oxidant and antioxidant status. Pancreatic beta-cells were examined by immunohistochemical methods. STZ induced a significant increase in lipid peroxidation and serum NO concentrations, and decreased antioxidant enzyme activity. NS treatment has been shown to provide a protective effect by decreasing lipid peroxidation and serum NO, and increasing antioxidant enzyme activity. Islet cell degeneration and weak insulin immunohistochemical staining was observed in rats with STZ-induced diabetes. Increased intensity of staining for insulin, and preservation of beta-cell numbers were apparent in the NS-treated diabetic rats. These findings suggest that NS treatment exerts a therapeutic protective effect in diabetes by decreasing oxidative stress and preserving pancreatic beta-cell integrity. Consequently, NS may be clinically useful for protecting beta-cells against oxidative stress.

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