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Prophylactic and antinociceptive effects of coenzyme q10 on diabetic neuropathic pain in a mouse model of type 1 diabetes

机译:辅酶q10对1型糖尿病小鼠模型中糖尿病性神经性疼痛的预防和镇痛作用

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Background: Oxidative stress is a key factor implicated in the development of diabetic neuropathy. This study evaluates the prophylactic and antinociceptive effects of the antioxidant coenzyme Q10 (CoQ10) on diabetes-induced neuropathic pain in a diabetic mouse model. Methods: Total 56 mice with type 1 diabetes induced by streptozotocin were used, 20 normal mice were used as control. Mechanical and thermal nociceptive behavioral assays were applied to evaluate diabetic neuropathic pain. Tissue lipid peroxidation, immunohistochemistry, reverse transcription, and polymerase chain reaction were used to evaluate the molecular mechanisms of CoQ10. Data are presented as mean ?? SEM. Results: CoQ10 administration was associated with reduced loss of body weight compared with nontreated diabetic mice, without affecting blood glucose levels. Low dose and long-term administration of CoQ10 prevented the development of neuropathic pain. Treatment with CoQ10 produced a significant dose-dependent inhibition of mechanical allodynia and thermal hyperalgesia in diabetic mice. Dorsal root ganglia, sciatic nerve, and spinal cord tissues from diabetic mice demonstrated increased lipid peroxidation that was reduced by CoQ10 treatment. CoQ10 administration was also noted to reduce the proinflammatory factors in the peripheral and central nervous system. Conclusions: The results of this study support the hypothesis that hyperglycemia induced neuronal oxidative damage and reactive inflammation may be pathogenic in diabetic neuropathic pain. CoQ10 may be protective by inhibiting oxidative stress and reducing inflammation by down-regulating proinflammatory factors. These results suggest that CoQ10 administration may represent a low-risk, high-reward strategy for preventing or treating diabetic neuropathy. ? 2013, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins.
机译:背景:氧化应激是糖尿病神经病变发展的关键因素。这项研究评估了抗氧化剂辅酶Q10(CoQ10)在糖尿病小鼠模型中对糖尿病引起的神经性疼痛的预防和镇痛作用。方法:采用链脲佐菌素诱导的1型糖尿病小鼠56只,作为正常小鼠20只。机械和热伤害行为分析用于评估糖尿病性神经性疼痛。组织脂质过氧化,免疫组织化学,逆转录和聚合酶链反应被用来评估辅酶Q10的分子机制。数据表示为平均值??扫描电镜结果:与未治疗的糖尿病小鼠相比,辅酶Q10的给药与体重减轻减少有关,而不会影响血糖水平。低剂量和长期服用辅酶Q10可预防神经性疼痛的发展。辅酶Q10的治疗对糖尿病小鼠的机械异常性疼痛和热痛觉过敏产生明显的剂量依赖性抑制作用。糖尿病小鼠的背根神经节,坐骨神经和脊髓组织表现出脂质过氧化增加,而CoQ10处理可减少脂质过氧化。还发现辅酶Q10的使用可以减少周围和中枢神经系统的促炎因子。结论:本研究结果支持以下假设:高血糖引起的神经元氧化损伤和反应性炎症可能是糖尿病性神经性疼痛的致病因素。辅酶Q10可通过抑制氧化应激并通过下调促炎因子来减轻炎症。这些结果表明,辅酶Q10的给药可能代表了预防或治疗糖尿病性神经病的低风险,高回报策略。 ? 2013年,美国麻醉医师学会有限公司。Lippincott Williams&Wilkins。

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