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褪黑素调节实验性糖尿病神经病变中的神经炎症和氧化应激:对 NF-κB 和 Nrf2 级联的影响。

Melatonin modulates neuroinflammation and oxidative stress in experimental diabetic neuropathy: effects on NF-κB and Nrf2 cascades.

机构信息

Molecular Neuropharmacology Laboratory, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Punjab, India.

出版信息

J Pineal Res. 2011 Mar;50(2):124-31. doi: 10.1111/j.1600-079X.2010.00821.x. Epub 2010 Nov 9.

Abstract

Melatonin exhibits an array of biological activities, including antioxidant and anti-inflammatory actions. Diabetic neuropathy is one of the complications of diabetes with a prevalence rate of 50-60%. We have previously reported the protective effect of melatonin in experimental diabetic neuropathy. In this study, we investigated the role of nuclear factor-kappa B (NF-κB) and nuclear erythroid 2-related factor 2 (Nrf2) in melatonin-mediated protection against streptozotocin-induced diabetic neuropathy. Melatonin at doses of 3 and 10 mg/kg was administered daily in seventh and eighth week after diabetes induction. Motor nerve conduction velocity and nerve blood flow were improved in melatonin-treated animals. Melatonin also reduced the elevated expression of NF-κB, IκB-α, and phosphorylated IκB-α. Further, melatonin treatment also reduced the elevated levels of proinflammatory cytokines (TNF-α and IL-6), iNOS and COX-2 in sciatic nerves of animals. The capacity of melatonin to modulate Nrf2 pathway was associated with increased heme oxygenase-1 (HO-1) expression, which strengthens antioxidant defense. This fact was also established by decreased DNA fragmentation (because inhibition of excessive oxidant-induced DNA damage) in the sciatic nerve of melatonin-treated animals. The results of this study suggest that melatonin modulates neuroinflammation by decreasing NF-κB activation cascade and oxidative stress by increasing Nrf2 expression, which might be responsible at least in part, for its neuroprotective effect in diabetic neuropathy.

摘要

褪黑素表现出多种生物活性,包括抗氧化和抗炎作用。糖尿病性神经病是糖尿病的并发症之一,其患病率为 50-60%。我们之前已经报道了褪黑素在实验性糖尿病性神经病中的保护作用。在这项研究中,我们研究了核因子-κB(NF-κB)和核红细胞 2 相关因子 2(Nrf2)在褪黑素介导的对抗链脲佐菌素诱导的糖尿病性神经病中的作用。在糖尿病诱导后的第 7 周和第 8 周,每天给予 3 和 10mg/kg 的褪黑素。在褪黑素处理的动物中,运动神经传导速度和神经血流得到改善。褪黑素还降低了 NF-κB、IκB-α 和磷酸化 IκB-α 的升高表达。此外,褪黑素治疗还降低了动物坐骨神经中促炎细胞因子(TNF-α和 IL-6)、iNOS 和 COX-2 的升高水平。褪黑素调节 Nrf2 途径的能力与血红素加氧酶-1(HO-1)表达的增加有关,这增强了抗氧化防御。这一事实也通过减少褪黑素处理动物坐骨神经中的 DNA 片段化(因为抑制了过量氧化剂诱导的 DNA 损伤)得到证实。这项研究的结果表明,褪黑素通过降低 NF-κB 激活级联和增加 Nrf2 表达来调节神经炎症和氧化应激,这可能至少部分解释了其在糖尿病性神经病中的神经保护作用。

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