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分子氢对糖尿病视网膜小胶质细胞的保护作用及其机制研究 被引量:3

A Study on the Protective Effect and Mechanism of Molecular Hydrogen on Diabetic Retinal Microglia Cells
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摘要 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/m L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。 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 mechanism of molecular hydrogen to inflammatory injury.
出处 《现代生物医学进展》 CAS 2016年第26期5015-5018,共4页 Progress in Modern Biomedicine
基金 黑龙江省青年科学基金项目(QC2011C119)
关键词 糖尿病视网膜病变 炎症 MIRNA TLR4 Diabetic retinopathy Hydrogen Inflammation miRNA TLR4
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  • 1Marcella, Nebbioso Federica, Pranno Nicola, et al. Lipoic acid inanimal models and clinical use in diabetic retinopathy[J]. Expert OpinPharmacother, 2013,4(13): 1829-1838.
  • 2Zhang B, Safa R, Rusciano D, et al. Epigallocatechin gallate, an activeingredient from green tea, attenuates damaging influences to theretina caused by ischemia/reperfusion [J]. Brain Res, 2007,1159:40-53.
  • 3Genfu, WuFen, Wan Huihui, Fu Ning,et al. A Matter of Timing:Contrasting Effects of Hydrogen Sulfide on Oxidative StressResponse in Shewanella oneidensis[J]. Journal of bacteriology, 2015,197(22): 3563-3572.
  • 4Ohta S. Recent progress toward hydrogen medicine: potential ofmolecular hydrogen for preventive and therapeutic applications [J].Cutt Pharm Des, 2011,17(22): 2241-2252.
  • 5Oharazawa H, Igarashi T, Yokota T, et al. Protection of the retina byrapid diffusion of hydrogen: administration of hydrogen-loaded eyedrops in retinal ischemia-reperftisioii injury[J]. Invest Ophthalmol VisSci,2010,51(1):487-492.
  • 6Vilhardt F. Microglia: phagocyte and glia cell [J]. Int J Biochem CellBiol, 2005,37(1): 17-21.
  • 7Min-Jin, Kim Se-Jae, Kim Sang Suk, et al. Hypochoeris radicataattenuatesLPS-induced inflammation by suppressing p38, ERK, andJNK phosphorylation in RAW 264.7 macrophagesfJ]. EXCLI journal,2014,13: 123-136.
  • 8Xu G,Zhang Z, Xing Y, et al. MicroRNA-149 negatively regulatesTLR-triggered inflammatory response inmacrophages by targetingMyD88[J]. Cell Biochem, 2014,115(5): 919-927.
  • 9Wei J, Huang X, Zhang Z, et al. MyD88 as a target of microRNA-203in regulation of lipopolysaccharide or BacilleCalmette-Guerininduced inflammatory response of macrophage RAW264.7 cells [J].Mol Immunol, 2013,55(3-4): 303-309.
  • 10Sonkoly E, Stahle M, Pivarcsi A. MicroRNAs and immunity: novelplayers in the regulation of normal immune fimction andinflammation[J]. Semin Cancer Biol, 2008,18(2): 131-140.

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