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The abnormal expression of long non-coding RNA (lncRNA) is closely related to disease progression. However, the role and mechanism of lncRNA H19 (lncH19) in sepsis-induced lung injury remain to be elucidated. Cercal ligation and puncture (CLP) mice models and lipopolysaccharide (LPS)-induced cell injury model was used to construct sepsis-induced lung injury  in vivo  and  in vitro . The expression of lncH19, microRNA (miR)-301a-3p, and adenylate cyclase 1 (Adcy1) mRNA was assessed using quantitative real-time PCR. The concentrations of inflammatory factors were determined by ELISA assay. Cell proliferation and apoptosis were determined using cell counting kit 8 assay, EdU staining, and flow cytometry. The protein expression of apoptosis markers and Adcy1 was examined by western blot analysis. Oxidative stress was assessed by detecting the contents of oxidative stress markers. The interaction between miR-301a-3p and lncH19 or Adcy1 was confirmed using RNA pull-down assay, dual-luciferase reporter assay, and RIP assay. LncH19 was lowly expressed in CLP mice models and LPS-induced cell injury models. Overexpressed lncH19 could alleviate CLP-induced lung injury in mice, as well as LPS-induced cell apoptosis, inflammation, and oxidative stress. MiR-301a-3p could be sponged by lncH19, and its overexpression could reverse the inhibition of lncH19 on LPS-induced cell injury. Adcy1 was a target of miR-301a-3p, and its expression was upregulated by lncH19. Silencing of Adcy1 could abolish the suppressive effect of the miR-301a-3p inhibitor on LPS-induced cell injury. LncH19 might inhibit sepsis-induced lung injury by acting as a sponge of miR-301a-3p to upregulate Adcy1.HIGHLIGHTSLncH19 overexpression relieves CLP-induced lung injury and LPS-induced cell injury.LncH19 directly sponges miR-301a-3p.MiR-301a-3p targets Adcy1. LncH19 overexpression relieves CLP-induced lung injury and LPS-induced cell injury. LncH19 directly sponges miR-301a-3p. MiR-301a-3p targets Adcy1.

LncRNA H19 acts as miR-301a-3p sponge to alleviate lung injury in mice with sepsis by regulating Adcy1