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褪黑素通过抑制细胞凋亡、炎症、氧化应激、DNA 损伤和线粒体损伤缓解大鼠脑出血后二次脑损伤。

Melatonin Alleviates Intracerebral Hemorrhage-Induced Secondary Brain Injury in Rats via Suppressing Apoptosis, Inflammation, Oxidative Stress, DNA Damage, and Mitochondria Injury.

机构信息

Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, Jiangsu Province, 215006, China.

出版信息

Transl Stroke Res. 2018 Feb;9(1):74-91. doi: 10.1007/s12975-017-0559-x. Epub 2017 Aug 1.

DOI:10.1007/s12975-017-0559-x
PMID:28766251
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5750335/
Abstract

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking. We designed this study to investigate the therapeutic effects and mechanisms of melatonin on the secondary brain injury (SBI) after ICH. An in vivo ICH model was induced via autologous whole blood injection into the right basal ganglia in Sprague-Dawley (SD) rats. Primary rat cortical neurons were treated with oxygen hemoglobin (OxyHb) as an in vitro ICH model. The results of the in vivo study showed that melatonin alleviated severe brain edema and behavior disorders induced by ICH. Indicators of blood-brain barrier (BBB) integrity, DNA damage, inflammation, oxidative stress, apoptosis, and mitochondria damage showed a significant increase after ICH, while melatonin reduced their levels. Meanwhile, melatonin promoted further increasing of expression levels of antioxidant indicators induced by ICH. Microscopically, TUNEL and Nissl staining showed that melatonin reduced the numbers of ICH-induced apoptotic cells. Inflammation and DNA damage indicators exhibited an identical pattern compared to those above. Additionally, the in vitro study demonstrated that melatonin reduced the apoptotic neurons induced by OxyHb and protected the mitochondrial membrane potential. Collectively, our investigation showed that melatonin ameliorated ICH-induced SBI by impacting apoptosis, inflammation, oxidative stress, DNA damage, brain edema, and BBB damage and reducing mitochondrial membrane permeability transition pore opening, and melatonin may be a potential therapeutic agent of ICH.

摘要

脑出血（ICH）是一种具有高死亡率和发病率的脑血管疾病，有效的治疗方法仍然缺乏。我们设计了这项研究，以探讨褪黑素对脑出血后继发性脑损伤（SBI）的治疗作用和机制。通过将自体全血注入 Sprague-Dawley（SD）大鼠右侧基底节来诱导体内 ICH 模型。原代大鼠皮质神经元用氧合血红蛋白（OxyHb）处理作为体外 ICH 模型。体内研究结果表明，褪黑素减轻了 ICH 引起的严重脑水肿和行为障碍。血脑屏障（BBB）完整性、DNA 损伤、炎症、氧化应激、细胞凋亡和线粒体损伤的指标在 ICH 后明显增加，而褪黑素降低了它们的水平。同时，褪黑素促进了 ICH 诱导的抗氧化指标表达水平的进一步增加。显微镜下，TUNEL 和尼氏染色显示褪黑素减少了 ICH 诱导的凋亡细胞数量。炎症和 DNA 损伤指标与上述指标表现出相同的模式。此外，体外研究表明，褪黑素减少了 OxyHb 诱导的凋亡神经元，并保护了线粒体膜电位。总之，我们的研究表明，褪黑素通过影响细胞凋亡、炎症、氧化应激、DNA 损伤、脑水肿和 BBB 损伤，降低线粒体膜通透性转换孔的开放，改善 ICH 引起的 SBI，褪黑素可能是 ICH 的一种潜在治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/85afa8d8ad55/12975_2017_559_Fig12_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/5b3aec1493af/12975_2017_559_Fig11_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/1912bd0948e4/12975_2017_559_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/b39f1d1441e6/12975_2017_559_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/a2d57a44960e/12975_2017_559_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/c3b6a16232f6/12975_2017_559_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/f8f76d330482/12975_2017_559_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/9933a759b434/12975_2017_559_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/22b7c3358d45/12975_2017_559_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/bc5eabb4511e/12975_2017_559_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/0ed7d2a0fdbc/12975_2017_559_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/5b3aec1493af/12975_2017_559_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff37/5750335/85afa8d8ad55/12975_2017_559_Fig12_HTML.jpg

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J Pineal Res. 2016-9-24

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