Long non-coding RNA ZFAS1 is down-regulated in sepsis. However, whether ZFAS1 participates in sepsis-induced cardiomyopathy (SIC) remains largely unknown. LPS injection to rats was used to establish an in vivo sepsis model, while LPS stimulation with H9C2 cell was used to mimic an in vitro sepsis-induced myocardial injury model. Western blots and quantitative RT-PCR were performed to evaluate protein and mRNA levels, respectively. ELISA was conducted to determine cytokine levels in supernatant. Flow cytometry was used to test apoptosis. Dual-luciferase assay was performed to validate binding between ZFAS1 and miR-34b-5p, miR-34b-5p and SIRT1. Our data revealed that ZFAS1 and SIRT1 were down-regulated, while miR-34b-5p was up-regulated in LPS-induced H9C2 cells. Inhibition of miR-34b-5p or overexpression of ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells. A mechanism study revealed that ZFAS1 sponged miR-34b-5p and thus elevated expression of SIRT1, which was prohibited by miR-34b-5p. ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells via the miR-34b-5p/SIRT1 axis, providing novel potential therapeutic targets for SIC.

长链非编码 RNA ZFAS1 在脓毒症中下调。然而，ZFAS1 是否参与败血症诱发的心肌病 (SIC) 仍然很大程度上未知。LPS 注射大鼠用于建立体内脓毒症模型，而 LPS 刺激 H9C2 细胞用于模拟体外脓毒症心肌损伤模型。分别进行蛋白质印迹和定量 RT-PCR 以评估蛋白质和 mRNA 水平。进行ELISA以确定上清液中的细胞因子水平。流式细胞仪用于检测细胞凋亡。进行双荧光素酶测定以验证 ZFAS1 与 miR-34b-5p、miR-34b-5p 和 SIRT1 之间的结合。我们的数据显示 ZFAS1 和 SIRT1 下调，而 miR-34b-5p 在 LPS 诱导的 H9C2 细胞中上调。抑制 miR-34b-5p 或过表达 ZFAS1 可减轻 LPS 刺激的 H9C2 细胞中的炎症反应和细胞凋亡。一项机制研究表明，ZFAS1 吸收了 miR-34b-5p，从而提高了 SIRT1 的表达，而 miR-34b-5p 抑制了 SIRT1 的表达。