Kanter Mehmet, Coskun Omer, Korkmaz Ahmet, Oter Sukru
Department of Medical Histology and Embryology, Faculty of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey.
Anat Rec A Discov Mol Cell Evol Biol. 2004 Jul;279(1):685-91. doi: 10.1002/ar.a.20056.
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.
本研究的目的是评估黑种草(NS)对链脲佐菌素(STZ)诱导的大鼠糖尿病β细胞损伤的可能保护作用。以50mg/kg的单次腹腔注射剂量注射STZ来诱导糖尿病。在给予STZ之前3天腹腔注射NS(0.2ml/kg/天),并且在整个4周的研究过程中持续进行这些注射。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)以及红细胞和胰腺组织丙二醛(MDA)水平(脂质过氧化的标志物),以确定氧化与抗氧化状态之间是否存在失衡。通过免疫组织化学方法检查胰腺β细胞。STZ导致脂质过氧化和血清NO浓度显著增加,并降低了抗氧化酶活性。NS治疗已显示出通过降低脂质过氧化和血清NO以及增加抗氧化酶活性来提供保护作用。在STZ诱导的糖尿病大鼠中观察到胰岛细胞变性和胰岛素免疫组织化学染色减弱。在NS治疗的糖尿病大鼠中,胰岛素染色强度增加以及β细胞数量得以保留是明显的。这些发现表明,NS治疗通过降低氧化应激和维持胰腺β细胞完整性在糖尿病中发挥治疗保护作用。因此,NS在临床上可能有助于保护β细胞免受氧化应激。