miRNA-335通过抑制HDAC3改善帕金森病的炎症反应研究

Research on miRNA-335 improves inflammatory response in Parkinson’s disease by inhibiting HDAC3

帕金森病(PD)是一种神经退行性疾病,但关于PD的发病机制还有待研究。文章探索了microRNA-335(miRNA-335)在PD炎症反应中的作用和机制。将细胞分成4组,分别为空白组、模型组(100μmol/L 6-羟多巴胺(6-OHDA))、pre-miRNA-335组(100μmol/L 6-OHDA+30 nmol/L miRNA-335前体寡核苷酸)和anti-miRNA-335组(100μmol/L 6-OHDA+30 nmol/L miRNA-335抑制剂),分别测定每组细胞活力、上清液炎症因子及miRNA-335、组蛋白脱乙酰酶3(HDAC3)和核转录因子-κB(NF-κB)的表达。与空白组相比,6-OHDA处理后,细胞活力、miRNA-335水平显著下降,而白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、HDAC3和NF-κB蛋白水平显著升高,而当miRNA-335过表达时,可以显著改善上述异常表达的指标,而敲低miRNA-335表达时,可以加剧上述指标的异常。miRNA-335可能通过靶基因HDAC3调控NF-κB的表达,从而调控炎症因子的表达,进而改善PD的炎症反应。

Parkinson’s disease(PD)is a neurodegenerative disease,but the pathogenesis of PD remains to be studied.This paper explores the role and mechanism of microRNA-335(miRNA-335)in the inflammatory response of PD.Divide the cells into four groups,namely blank group,model group(100μmol/L 6-hydroxydopamine(6-OHDA)),pre-miRNA-335 group(100μmol/L 6-OHDA+30 nmol/L miRNA-335 precursor oligonucleusnucleotide)and anti-miRNA-335 group(100μmol/L 6-OHDA+30 nmol/L miRNA-335 inhibitor),the cell viability,supernatant inflammatory factors and miRNA-335,histone deacetylase 3(HDAC3)and nuclear transcription factor-κB(NF-κB)in each group were measured respectively expression.Compared with the blank group,after 6-OHDA treatment,cell viability and miRNA-335 levels were significantly decreased,while interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),HDAC3 and NF-κB protein level was significantly increased,and when miRNA-335 was overexpressed,the above indicators of abnormal expression could be significantly improved,while knockdown of miRNA-335 expression could aggravate the abnormality of the above indicators.miRNA-335 may regulate the expression of NF-κB through the target gene HDAC3,then regulating the expression of inflammatory factors,thereby improving the inflammatory response of PD.