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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Melatonin protects against neurobehavioral and mitochondrial deficits in a chronic mouse model of Parkinson's disease.
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Melatonin protects against neurobehavioral and mitochondrial deficits in a chronic mouse model of Parkinson's disease.

机译：在帕金森氏病的慢性小鼠模型中，褪黑素可预防神经行为和线粒体缺陷。

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Neuronal oxidative stress and mitochondrial dysfunction have been implicated in Parkinson's disease. Melatonin is a natural antioxidant and free radical scavenger that has been shown to effectively reduce cellular oxidative stress and protect mitochondrial functions in vitro. However, whether melatonin is capable of slowing down the neurodegenerative process in animal models of Parkinson's disease remains controversial. In this research, we examined long-term melatonin treatment on striatal mitochondrial and dopaminergic functions and on animal locomotor performance in a chronic mouse model of Parkinson's disease originally established in our laboratory by gradually treating C57BL/6 mice with 10 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (15 mg/kg, s.c.) and probenecid (250 mg/kg, i.p.) over five weeks. We report here that when the chronic Parkinsonian mice were pre-treated and continuously treated with melatonin (5mg/kg/day, i.p.) for 18 weeks, the defects of mitochondrial respiration, ATP and antioxidant enzyme levels detected in the striatum of chronic Parkinson's mice were fully preempted. Meanwhile, the striatal dopaminergic and locomotor deficits seen in the chronic Parkinson's mice were partially and significantly forestalled. These results imply that long-term melatonin is not only mitochondrial protective but also moderately neuronal protective in the chronic Parkinson's mice. Melatonin may potentially be effective for slowing down the progression of idiopathic Parkinson's disease and for reducing oxidative stress and respiratory chain inhibition in other mitochondrial disorders.
机译：神经元氧化应激和线粒体功能障碍与帕金森氏病有关。褪黑素是一种天然的抗氧化剂和自由基清除剂，已被证明可以有效降低细胞的氧化应激并在体外保护线粒体功能。然而，褪黑素是否能够减慢帕金森氏病动物模型的神经变性过程仍存在争议。在这项研究中，我们研究了褪黑素对纹状体线粒体和多巴胺能功能以及动物帕金森病慢性动物模型的运动能力的长期治疗，该模型最初是在我们实验室中建立的，通过逐步用10剂量的1-甲基-在五周内使用4-苯基-1,2,3,6-四氢吡啶（15 mg / kg，sc）和丙磺舒（250 mg / kg，ip）。我们在这里报告，当慢性帕金森氏小鼠经过预处理并连续用褪黑激素（5mg / kg /天，腹腔注射）治疗18周时，在慢性帕金森氏小鼠纹状体中检测到线粒体呼吸，ATP和抗氧化酶水平的缺陷被完全抢占。同时，在慢性帕金森病小鼠中发现的纹状体多巴胺能和运动功能障碍被部分地和显着地阻止了。这些结果表明，长期褪黑素不仅对线粒体具有保护作用，而且在慢性帕金森氏病小鼠中具有中度神经元保护作用。褪黑激素可能有效地减慢了特发性帕金森氏病的进程，并减轻了其他线粒体疾病的氧化应激和呼吸链抑制作用。

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