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首页> 外文期刊>BMC Neuroscience >Effects of melatonin on the nitric oxide system and protein nitration in the hypobaric hypoxic rat hippocampus
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Effects of melatonin on the nitric oxide system and protein nitration in the hypobaric hypoxic rat hippocampus

机译：褪黑素对低压缺氧大鼠海马一氧化氮系统和蛋白质硝化的影响

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Background It is well documented that the nitric oxide (NO) might be directly involved in brain response to hypobaric hypoxia, and could contribute to memory deficiencies. Recent studies have shown that melatonin could attenuate hypoxia or ischemia-induced nerve injuries by decreasing the production of free radicals. The present study, using immunohistochemical and immunoblot methods, aimed to explore whether melatonin treatment may affect the expression of nitric oxide system and protein nitration, and provide neuroprotection in the rat hippocampus injured by hypobaric hypoxia. Prior to hypoxic treatment, adult rats were pretreated with melatonin (100?mg/kg, i.p.) before they were exposed to the altitude chamber with 48?Torr of the partial oxygen concentration (pO2) for 7?h to mimic the ambience of being at 9000?m in height. They were then sacrificed after 0?h, 1, and 3?days of reoxygenation. Results The results obtained from the immunohistochemical and immunoblotting analyses showed that the expressions of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitrotyrosine (Ntyr) and Caspase 3 in the hypoxic hippocampus were increased from 0?h to 3?days of reoxygenation. Interestingly, the hypoxia-induced increase of nNOS, eNOS, iNOS, Ntyr and Caspase 3 protein expression was significantly depressed in the hypoxic rats treated with melatonin. Conclusions Activation of the nitric oxide system and protein nitration constitutes a hippocampal response to hypobaric hypoxia and administration of melatonin could provide new therapeutic avenues to prevent and/or treat the symptoms produced by hypobaric hypoxia.
机译：背景大量文献证明，一氧化氮（NO）可能直接参与大脑对低压缺氧的反应，并可能导致记忆缺陷。最近的研究表明，褪黑激素可以通过减少自由基的产生来减轻缺氧或局部缺血引起的神经损伤。本研究使用免疫组化和免疫印迹方法，旨在探讨褪黑激素治疗是否会影响一氧化氮系统的表达和蛋白硝化，并为低压低氧所致的海马提供神经保护。低氧治疗前，成年大鼠用褪黑素（100？mg / kg，ip）进行预处理，然后暴露于海拔48托的部分氧浓度（pO 2 ）达7升？h模仿在9000？m高处的氛围。然后在再充氧0？h，1和3天后将它们处死。结果免疫组织化学和免疫印迹分析结果表明，低氧海马中神经元一氧化氮合酶（nNOS），内皮型一氧化氮合酶（eNOS），诱导型一氧化氮合酶（iNOS），硝基酪氨酸（Ntyr）和胱天蛋白酶3的表达复氧时间从0小时增加到3天。有趣的是，在用褪黑素治疗的低氧大鼠中，低氧诱导的nNOS，eNOS，iNOS，Ntyr和Caspase 3蛋白表达的增加被显着抑制。结论一氧化氮系统的活化和蛋白质的硝化作用构成了对低压缺氧的海马反应，褪黑激素的给药可为预防和/或治疗低压缺氧所产生的症状提供新的治疗途径。

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