Curcumin alleviated lipopolysaccharide-evoked H9c2 cells damage via suppression of intercellular adhesion molecule 1/CD40/NF-κB signaling.

Abstract

Curcumin has been reported to have many benefits, including anti-inflammatory, anti-cancer, and so on. In this research, we aimed to investigate the function of curcumin on lipopolysaccharide (LPS)-injured H9c2 cells. H9c2 cells stimulated by LPS mimic the in vitro model of myocarditis injury. Comparative Toxicogenomics Database (CTD) was applied to detect the genes associated with curcumin. GEO database was used to analyze Intercellular Adhesion Molecule 1 (ICAM1) and CD40 expression in myocarditis patients. KEGG enrichment analysis was employed to investigate the meaningful pathways related to differentially expressed genes. Cell proliferation, apoptosis, expression of ICAM1/CD40/P65- NF-κB, and level of TNF-α, IL-6, and IL-10 were observed by cell counting kit-8, flow cytometry and western blotting assays, ELISA assay, respectively. After curcumin treatment, the decreased activity of H9c2 cells evoked by LPS was improved. ICAM1 and CD40, which highly expressed in myocarditis patients, were identified as targets of curcumin and negatively regulated by curcumin. Inhibition of ICAM1 or CD40 strengthened the protective effect of curcumin on LPS-evoked H9c2 cells damage, accompanied by increased cell viability and decreased cell apoptosis and inflammation. Additionally, addition of curcumin or depletion of ICAM1/CD40 suppressed p-P65 NF-κB expression. Curcumin mitigated LPS-evoked H9c2 cells damage by suppression of ICAM1/CD40/NF-κB, providing a potential molecular mechanism for the clinical application of curcumin.