LncRNA small nucleolar RNA host gene 16 reduces sepsis‐induced myocardial damage by regulating miR ‐421/suppressor of cytokine signaling 5 axis

Currently, sepsis‐induced cardiomyopathy (SIC) remains as one of the most critical clinical syndromes in terminally ill patients. Noncoding RNAs (including microRNAs and long noncoding RNAs) are implicated in both the onset and development of SIC. We herein investigated the functional role and molecular target of long noncoding RNA small nucleolar RNA host gene 16 (SNHG16) in an in vitro SIC model of H9c2 myocardial cells. We used lipopolysaccharide (LPS) as endotoxin to treat H9c2 cells to mimic SIC damages. Cell Counting Kit 8 and apoptosis assay were performed to assess cell proliferation and cell death. Quantitative real‐time‐PCR and Western blot were employed to examine gene expression level at mRNA and protein level. Dual luciferase assay is used to validate the functional interactions between SNHG16/mi‐R421 and miR‐421/suppressor of cytokine signaling 5 (SOCS5). Inflammatory cytokines were measured by ELISA. Superoxide dismutase and malondialdehyde measurement was performed to assess oxidative stress, which was further confirmed by 2′,7′‐dichlorofluorescin diacetate staining. Our data demonstrated that in the LPS‐induced sepsis model of myocardial cells, SNHG16 overexpression downregulated the expression level of miR‐421, which sustained the expression of SOCS5 to alleviate the adverse effects of LPS, such as apoptosis, pro‐inflammatory cytokines, and oxidative stress. Our data suggest that SNHG16 functions as a ceRNA to maintain SOCS5 level by targeting miR‐421, thereby attenuating LPS‐induced myocardial cell damages. Targeting miR‐421 or modulating lncRNA SNHG16 level may be leveraged as a beneficial strategy against sepsis‐induced cellular damage in cardiomyocytes.