被撤回的出版物: MicroRNA-208-5p regulates myocardial injury of sepsis mice via targeting SOCS2-mediated NF-κB/HIF-1α pathway (Retracted article. See vol. 117, 2023)

Background: Accumulating evidence has revealed the roles of microRNAs (miRs) in sepsis, hence, the aim of the present study was to investigate whether miR-208a-5p affects sepsis whilst attempting to elucidate the me-chanisms by which the suppressors of cytokine signaling 2 (SOCS2)-mediated nuclear factor-kappaB/hypoxia-inducible factor-1 alpha (NF-kappa B/HIF-1 alpha) pathway is implicated in this process. Methods: The sepsis model was established by cecal ligation and puncture in mice. Serum levels of myocardial enzyme cardiac Troponin-I (cTnI) and brain natriuretic peptide (BNP) in mice were measured. Malondialdehyde (MDA), lactate dehydrogenase (LDH) activity, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), NF-kappa B p65, HIF-1 alpha and superoxidedismutase (SOD) activity in myocardial tissues were determined. Furthermore, the swelling degree of mitochondria and the apoptosis of cardiomyocytes was measured. The expression of miR-208a-5p, SOCS2, Bcl-2, Bax, NF-kappa B p65 and HIF-1 alpha in myocardial tissues of mice were detected. Results: Down-regulation of miR-208a-5p and up-regulation of SOCS2 raised the activity of SOD, while reduced the activity of LDH and MDA and the concentrations of cTnI, BNP, TNF-alpha, IL-6, NF-kappa B p65 and HIF-1 alpha in mice with sepsis. Down-regulated miR-208a-5p and up-regulated SOCS2 reduced degree of mitochondria swelling, and suppressed cardiomyocytes apoptosis in mice with sepsis. MiR-208a-5p, NF-kappa B p65 and HIF-1 alpha expression were raised while SOCS2 expression was depressed in myocardial tissues of mice with sepsis. Conclusion: This study suggests that high expression of SOCS2 or inhibition of miR-208a-5p alleviates the myocardial injury of sepsis mice via modulating NF-kappa B/HIF-1 alpha pathway, which are potential candidate markers and therapeutic targets for sepsis mice.