Abstract
Objective To investigate the role of micro RNA-124(miR-124)in regulating activation of microglias and secretion of pro-inflammation cytokines and its potential mechanism. Methods (1)BV-2 cells were exposed to different concentration of lipopolysaccharide(LPS)for different durations; relative expression level of miR-124 was detected by real time-quantitative PCR(RT-qPCR).(2)The BV-2 cells were divided into four groups: PBS group, LPS group, LPS + ctrl-simulant group and LPS + miR-124 simulant group. Protein and mRNA expressions of inflammatory factors(tumor necrosis factor[TNF]-α and interleukin[IL]1-β)were evaluated by RT-qPCR and ELISA. Expressions of p38α, phosphorylated(p)-p38α, ERK and p-ERK were detected by Western blotting.(3)Besides the above groups, four groups were added: LPS + VX702 group, LPS + miR-124 inhibitor group,LPS + VX702 + miR-124 simulant group and LPS + VX702 + miR-124 inhibitor group; pretreatment with p38α specific inhibitor VX702 was given to the BV-2 cells, the latter two groups were given miR-124 simulant or miR-124 inhibitor, and LPS was used to activate the cells; the expressions of TNF-α and IL-1β were evaluated by ELISA. Results (1)As compared with control group, miR-124 was significantly down-regulated in LPS-stimulated BV-2 cells(P 0.05).(3)The TNF-α and IL-1β levels between LPS+VX702 group and LPS+VX702+miR-124 simulant group were not significantly different(P>0.05); those between the LPS+VX702+miR-124 inhibitor group and the LPS + VX702 group were not significantly different(P>0.05). Conclusion The miR-124 is down-regulated in LPS-activated BV-2 cells and miR-124 could suppress the secretion of pro-inflammatory mediators by targeting to p38α. Key words: Neuroinflammation; Microglia; Micro RNA-124; p38α
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