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首页> 外文期刊>Drug Design, Development and Therapy >Melatonin Alleviates Neuronal Damage After Intracerebral Hemorrhage in Hyperglycemic Rats
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Melatonin Alleviates Neuronal Damage After Intracerebral Hemorrhage in Hyperglycemic Rats

机译：褪黑激素缓解了高血糖大鼠脑出血后的神经元损伤

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Background: This study sought to investigate a novel effect of melatonin in reducing brain injury in an in vivo hyperglycemic intracerebral hemorrhage (ICH) model and further explore the mechanisms of protection. Methods: Hyperglycemia ICH was induced in Sprague-Dawley rats by streptozocin injection followed by autologous blood injection into the striatum. A combined approach including RNA-specific depletion, electron microscopy, magnetic resonance, Western blots, and immunohistological staining was applied to quantify the brain injuries after ICH. Results: Hyperglycemia resulted in enlarged hematoma volume, deteriorated brain edema, and aggravated neuronal mitochondria damage 3 days after ICH. Post-treatment with melatonin 2 hours after ICH dose-dependently improved neurological behavioral performance lasting out to 14 days after ICH. This improved neurological function was associated with enhanced structural and functional integrity of mitochondria. Mechanistic studies revealed that melatonin alleviated mitochondria damage in neurons via activating the PPARδ/PGC-1α pathway. Promisingly, melatonin treatment delayed until 6 hours after ICH still reduced brain edema and improved neurological functions. Melatonin supplementation reduces neuronal damage after hyperglycemic ICH by alleviating mitochondria damage in a PPARδ/PGC-1α-dependent manner. Conclusion: Melatonin may represent a therapeutic strategy with a wide therapeutic window to reduce brain damage and improve long-term recovery after ICH.
机译：背景：本研究试图探讨褪黑激素在体内高血糖脑出血（ICH）模型中降低脑损伤的新效果，进一步探索了保护机制。方法：通过链脲酶注射液在Sprague-Dawley大鼠中诱导高血糖Ich，然后通过自体血液注射到纹状体中。施用包括RNA特异性耗竭，电子显微镜，磁共振，蛋白质印迹和免疫组织学染色的组合方法，以量化ICH后的脑损伤。结果：高血糖导致血肿体积扩大，脑水肿恶化，治疗后3天加重神经元线粒体损伤。用褪黑素治疗后2小时后依赖于ICH后持续到14天后的神经系统行为性能。这种改进的神经功能与线粒体的增强结构和功能完整性有关。机械研究表明，褪黑素通过激活PPARδ/ PGC-1α途径缓解了神经元的线粒体损伤。承诺，褪黑激素治疗延迟至6小时后，在脑水肿降低和改善神经功能后。褪黑激素补充通过减轻PPARδ/ PGC-1α依赖性方式的线粒体损伤来减少高血糖症后的神经元损伤。结论：褪黑激素可以代表一种具有宽治疗窗的治疗策略，以降低脑损伤，并在ICH后改善长期恢复。

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