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We aimed to elucidate the roles of the long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3)/microRNA-7b (miR-7b)/NLR pyrin domain containing 3 (NLRP3) axis in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Mouse alveolar macrophage NR8383 and mice were administrated with LPS to establish ALI models in vitro and in vivo . NLRP3 was silenced while miR-7b was overexpressed in LPS-induced NR8383 cell model of ALI. The interleukin-18 (IL-18) and IL-1β, as well as caspase-1, tumor necrosis factor-α (TNF-α) and IL-6 protein levels were assayed. To further investigate the underlying mechanisms of NLRP3 in ALI, lncRNA MEG3 was silenced and miR-7b was overexpressed in LPS-induced NR8383 cell model of ALI, after which in vivo experiments were performed for further verification. NLRP3 was highly expressed in LPS-induced NR8383 cell model of ALI. Silencing NLRP3 or overexpressing miR-7b inhibited IL-18 and IL-1β, as well as caspase-1, TNF-α and IL-6. LncRNA MEG3 could sponge miR-7b, and lncRNA MEG3 silencing or miR-7b overexpression downregulates NLRP3 expression, thus reducing IL-18 and IL-1β, as well as caspase-1, TNF-α and IL-6 levels. The in vivo experiments further confirmed the aforementioned findings. Silencing lncRNA MEG3 augments miR-7b binding to NLRP3 and downregulates NLRP3 expression, which ultimately improves LPS-induced ALI.

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Silencing of long non-coding RNA MEG3 alleviates lipopolysaccharide-induced acute lung injury by acting as a molecular sponge of microRNA-7b to modulate NLRP3