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目的：研究分子氢对糖尿病视网膜小胶质细胞的保护作用及其可能机制。方法：采用100 ng/mL的LPS诱导视网膜小胶质细胞，同时将两组细胞分别置于正常培养环境和含有饱和氢培养环境下培养36 小时。RT-PCR 检测小胶质细胞中miR-9、miR-21 和 miR-199 的表达。Western Blot测定TLR4 信号途径相关蛋白的表达。结果：miR-9、miR-21 在分子氢作用后明显下调，而miR-199 在分子氢作用后下调不明显。并且，小胶质细胞活化后TLR4 途径相关信号蛋白的表达增加，在分子氢处理后Myd88 和IKKβ蛋白的表达明显减少，而NF-κB蛋白的表达前后没有明显的变化。结论：分子氢对视网膜小胶质细胞的炎症损伤具有明显的保护作用，氢作为一种信号分子对Myd88 介导的TLR4 炎症信号通路的调节及通路中部分miRNA 的调节作用可能是其抗炎作用的机制。

英文摘要:

Objective:Molecular hydrogen was proved to be of neuroprotective effect to the retinal injury through its innate regulatory mechanism and to provide the evidence that microRNAs are involved in the molecular pathogenesis of diabetic retinopathy.Methods:In present study, using Lipopolysaccharide (LPS)-activated retinal microglia model, we explored the potential mechanism of molecular hydrogen in regulation of miRNA expression and signal-modulating activities. Retinal microglia was activated by LPS, and then was treated with hydrogen-saturated medium or normal medium without hydrogen. qRT-PCR was used to detect the expression difference of miR-9, miR-21 and miR-199 between these two groups.Results:The results demonstrated a dramatic down-regulation of miR-9 and miR-21 by hydrogen treatment, while up-regulation of miR-199. Furthermore, we also detected the expression of LPS-induced signaling proteins including Myd88, IKKβ, NF-κb, and PDCD4 by Western Blot. The data showed that the expression of Myd88 and IKKβ were decreased after hydrogen treatment, whereas PDCD4 was increased, and there was no significant change in NF-κB expression.Conclusion:The results in present study indicated that miR-9, miR-199 and miR-21 might play an important role in the anti-inflammatory regulation of molecular hydrogen in LPS-activated microglias which will help further to explain the protective mechanismof molecular hydrogen to inflammatory injury.

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