[lncRNA-HOTAIR inhibits the proliferation of H9c2 rat cardiomyocytes induced by lipopolysaccharide and promotes inflammation through targeting negative regulation of miR-1-3p].

Objective To investigate whether long non-coding RNA-HOX transcript antisense intergenic RNA (lncRNA-HOTAIR) regulates the inflammatory response of sepsis by targeting microRNA miR-1-3p. Methods 0.5 μg/mL lipopolysaccharide (LPS) was used to induce cardiomyocytes of H9c2 rats to establish a septic cardiomyocyte injury model. H9c2 cells were divided into control group, LPS group, and LPS combined with HOTAIR small interfering RNA negative control (si-NC) group, LPS combined with HOTAIR small interfering RNA (si-HOTAIR) group, LPS combined with miR-1-3p negative control (miR-NC) group, LPS combined with miR-1-3p group, LPS combined with si-HOTAIR and miR-1-3p inhibitor negative (anti-miR-NC) group, and LPS combined with siHOTAIR and anti-miR-1-3p group. Real-time quantitative PCR was used to determine the expression of HOTAIR and miR-1-3p, CCK-8 assay was used to detect cell proliferation, and Western blotting was used to analyze antigen KI-67 (ki67), P21, B-cell lymphoma 2 (Bcl2), Bcl2-related X protein (BAX) protein expression. Flow cytometry was performed to evaluate cell apoptosis. ELISA was used to determine the inflammatory factor interleukin 6(IL-6) and tumor necrosis factor-α (TNF-α) levels. The dual luciferase report experiment analyzes the targeting relationship between HOTAIR and miR-1-3p. Results The expression of HOTAIR in H9c2 cells of the LPS group was higher than that of the control group, and the expression of miR-1-3p was lower than that of the control group. Compared with the LPS combined with si-NC group, the LPS combined with si-HOTAIR treated H9c2 cell proliferation activity, presenting increased ki67 and Bcl2 expression, as well as decreased level of P21 expression, apoptosis rate, BAX expression, IL-6 and TNF-α. HOTAIR targets and regulates the expression of miR-1-3p. Compared with the LPS combined miR-1-3p group, the proliferation activity, ki67, Bcl2 expression of H9c2 cells increased in the LPS combined miR-NC group, and the P21 expression, apoptosis rate, BAX expression, IL-6, and TNF-α levels decreased. Compared with the LPS combined with si-HOTAIR and anti-miR-NC group, the H9c2 cell proliferation activity in the LPS combined with siHOTAIR and anti-miR-1-3p group descended, and the expression of ki67 and Bcl2 decreased, while the expression of P21, BAX, apoptosis, IL-6 and TNF-α levels increased. Conclusion HOTAIR negatively regulates the expression of miR-1-3p, inhibits LPS-induced cardiomyocyte H9c2 proliferation, and induces cell apoptosis and inflammation.