Investigation on the association and potential mechanism of lncRNA SNHG4 in perioperative respiratory adverse events of children

This research aimed to investigate the correlation between perioperative respiratory adverse events (PRAE) and postoperative serum SNHG4 levels, and preliminarily explore the potential regulatory mechanism of SNHG4 in an inflammatory lung injury cell model. Among the children undergoing general anesthesia surgery, this study included 122 children with PRAE. 104 patients without PRAE were assigned to the control group. RT-qPCR was employed to quantify the level of SNHG4 in serum. Receiver operating characteristic (ROC) curve and binary logistic regression were performed to preliminarily assess the association between PRAE occurrence and postoperative SNHG4 level. In vitro, human pulmonary microvascular endothelial cells (HPMECs) were treated with lipopolysaccharide (LPS). CCK-8 assay and flow cytometry were conducted to detect cell viability and apoptosis, respectively, and ELISA was applied to quantify the secretion of inflammatory cytokines. The level of SNHG4 in the PRAE group was significantly lower than that in the control group. Postoperative serum SNHG4 level was significantly correlated with the occurrence of PRAE. In LPS-stimulated HPMECs, restoring SNHG4 expression significantly enhanced cell viability, decreased the apoptotic rate, and reduced the secretion of pro-inflammatory cytokines. Dual-luciferase reporter assays confirmed the targeting relationship between SNHG4 and miR-449c-5p. Rescue experiments further demonstrated that overexpression of miR-449c-5p could partially reverse the biological effects of SNHG4 overexpression on LPS-induced HPMECs. A statistically significant association was observed between PRAE and postoperative serum SNHG4 level. In injured pulmonary endothelial cells, SNHG4 shows a significant correlation with inflammatory responses, which is linked to its targeting effect on miR-449c-5p.