LncRNA SNHG12 Inhibition Based on Microsystem Cell Imaging Technology Protects the Endothelium from LPS-Induced Inflammation by Inhibiting the Expression of miR-140-3p Target Gene fndc5.

Abstract

Acute lung injury (ALI) is a serious disease with a high incidence rate, characterized by uncontrolled inflammation and apoptosis. At present, long-chain noncoding RNA (lncRNA) is a noncoding RNA with a length of more than 200 nucleotides. It plays an important role in ALI, cell cycle regulation, cell differentiation regulation, and many other life activities. Therefore, the current focus is to identify and evaluate the possible functions and potential molecular mechanisms of lncRNA small nuclear host gene 12 (SNHG12). Lipopolysaccharide (LPS)-induced mice model and in vitro cell model were established. Gene knockout is to use the principle of DNA homologous recombination to replace the target gene fragment with the designed homologous fragment, so as to achieve the purpose of gene knockout. The relationship between lncRNA SNHG12 expression and ALI was studied through knockdown and overexpression experiments. The qRT-PCR, ROS, immunohistochemistry, histopathology, TUNEL, and cell permeability tests were performed to further verify the possible targets and mechanisms of action. The expression of lncRNA SNHG12 in lung tissue was lower than that in normal tissue. The results showed that lncRNA SNHG12 could reduce lung cell injury and inflammatory cytokines induced by ALI. Bioinformatics analysis showed that lncRNA SNHG12 interacted with miR-140-3p. Subsequent experiments confirmed the link between lncRNA SNHG12, miR-140-3p, and fndc5. Furthermore, this study indicates that lncRNA SNHG12 has a key function in ALI. The results of this study demonstrated the role of lncRNA SNHG12 in the pathological process of ALI and provided a reference for developing novel anti-ALI treatments so that patients can get timely treatment, avoid causing multiple organ failure, and will not endanger their life safety.