Excessive inflammation is predominantly involved in the pathogenesis of acute lung injury (ALI). Recently, microRNAs (miRNAs) have been shown to act as an important regulator of inflammation. Hence, we investigated the levels of miR-182-5p and its functional role about regulating inflammation in LPS-induced ALI mice and RAW264.7 cells. Here, LPS induced-ALI model was established in male mice. By qRT-PCR, we found that the expression of miR-182-5p was significantly downregulated in lung tissue and bronchoalveolar lavage fluid (BALF), as well as decreased in LPS-treated RAW264.7 cells. In vitro, overexpression of miR-182-5p suppressed the inflammatory response, as evidenced by reduction of pro-inflammatory cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α). Further experiments revealed that toll-like receptor 4 (TLR4) was the target of miR-182-5p, which was confirmed by luciferase activity assay. Moreover, RAW264.7 cells transfected with pcDNA-TLR4 plasmid abrogated the protective effects of miR-182-5p against LPS-induced inflammatory response. Additionally, we observed that overexpression of miR-182-5p blocked LPS-induced activation of the NF-κB signaling pathway by targeting TLR4. Collectively, the findings of our study indicate that miR-182-5p inhibits the inflammatory response by modulating TLR4/NF-κB signaling pathway in LPS-treated RAW264.7 cells.
Keywords: Acute lung injury; MicroRNA-182-5p; TLR4/NF-κB signaling pathway; inflammatory response.
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