miR-141 alleviates LPS-induced inflammation injury in WI-38 fibroblasts by up-regulation of NOX2.

AIMS: The roles of miR-141 in various types of cancers and inflammatory bowel diseases are researched, whereas, little information about its function in lung inflammation is available. This study was designed to explore the effect of miR-141 on inflammation injury in WI-38 cells, possibly providing basis for targeted therapeutic strategy for treatment of infantile pneumonia.

MAIN METHODS: WI-38 cells were treated with LPS to construct cell model with inflammation injury. Expressions of miR-141 and NOX2 were altered by transfection assay and expressions of them were detected by qRT-PCR or Western blot. Cell viability and apoptosis were evaluated by CCK-8 assay and flow cytometry, respectively. The tested pro-inflammatory factors were analyzed by qRT-PCR and Western blot; and their productions were quantified by ELISA. Main proteins participating in regulation of apoptosis, p38 MAPK pathway and NF-κB pathway were analyzed by Western blot.

KEY FINDINGS: miR-141 was down-regulated in LPS-treated cells and elevating miR-141 level reduced inflammation extent of WI-38 cells by promoting viability, inhibiting apoptosis, and inhibiting production of tested pro-inflammatory cytokines. NOX2 was up-regulated by miR-141 overexpression. NOX2 silence impaired the cell-protective effect of miR-141. miR-141 inhibited LPS-induced activations of p38 MAPK and NF-κB pathways, which was also mediated by NOX2.

SIGNIFICANCE: miR-141 alleviated LPS-induced inflammation injury in WI-38 fibroblasts by up-regulating NOX2 and further inhibiting p38 MAPK and NF-κB pathways.