Effects and early diagnostic value of lncRNA H19 on sepsis-induced acute lung injury.

Abstract

Sepsis is an immune disease induced by microbial invasion. The molecular mechanism and value of long non-coding H19 (lncRNA H19) in sepsis remain largely unknown. The present study aimed to investigate the effects and early diagnostic value of lncRNA H19 on sepsis-induced acute lung injury (ALI). Serum samples from 85 septic patients and 76 healthy individuals were collected, and the expression of lncRNA H19 was assessed by the quantitative polymerase chain reaction (qPCR). Sprague-Dawley (SD) rats were subjected to cecal ligation and puncture (CLP) in order to construct models of sepsis-induced ALI. A total of 18 successfully modeled rats were randomly allocated into an lncRNA H19-ad group and a model group, and another 9 healthy SD rats from the same batch were selected as a control group. The samples of serum and lung tissue were collected. lncRNA H19 expression was quantified by qPCR, and levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-17, caspase-3, caspase-9, B-cell lymphoma-2 (Bcl-2), and BCL2-associated X (Bax) were measured by western blotting. A receiver operating characteristic (ROC) curve was employed to assess the diagnostic value of lncRNA H19 for septic patients. lncRNA H19 was downregulated in sepsis. Upregulation of lncRNA H19 inhibited TNF-α, IL-6, IL-17, caspase-3, caspase-9 and Bax and increased Bcl-2. The AUC of lncRNA H19 for early diagnosis of sepsis was 0.8197 (95% CI, 0.77 to 0.91). lncRNA H19 alleviated sepsis-induced ALI by inhibiting pulmonary apoptosis and inflammation, serving as a biochemical marker and therapeutic target for sepsis.