Mef2c Alleviates Acute Lung Injury In Cecal Ligation And Puncture (Clp)-Induced Sepsis Rats By Up-Regulating Aqp1

Background: Sepsis is a systemic inflammatory response syndrome and leads to patient's death. Objective: To investigate the effect of myocyte enhancer factor 2 (MEF2C) on acute lung injury (ALI) with sepsis and its possible mechanism.Material and Methods: The cecal ligation and puncture (CLP)-induced sepsis rat model was established. The lung injury was determined by lung wet-dry weight ratio, the concentration of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), Interlukin (IL)-6, IL-1 beta, and IL-10, were measured by the enzyme-linked-immunosorbent serologic assay kit. The cell apoptosis was detected by TUNEL staining assay.Results: Interestingly, MEF2C was down-regulated in this model. Moreover, adeno-associated virus (AAV)-MEF2C treatment markedly suppressed TNF-alpha, IL-1 beta, and IL-6 concentrations but promoted IL-10 concentration in serum in CLP-challenged rats. Besides, overexpression of MEF2C alleviates CLP-induced lung injury. Interestingly, AAV-MEF2C treatment was confirmed to suppress apoptosis in CLP-induced sepsis rats as well as promote aquaporin APQ1 expression. Mechanistically, the rescue experiments indicated that MEF2C alleviated CLP-induced lung inflammatory response and apoptosis via up-regulating AQP1.Conclusion: In summary, overexpression of MEF2C suppressed CLP-induced lung in.ammatory response and apoptosis via up-regulating AQP1, providing a novel therapeutic target for sepsis-induced ALI. (C) 2021 Codon Publications. Published by Codon Publications.