Mechanism Underlying P-Coumaric Acid Alleviation of Lipid Accumulation in Palmitic Acid-Treated Human Hepatoma Cells

The protective effect and mechanism of action of p-coumaric acid for alleviating palmitic acid (PA)-induced hepatocyte injury were investigated using a PA-induced human hepatoma cell (HepG2)-based hepatocellular injury model and MTT cell viability determinations. Additionally GSH content and CAT activity were detected using commercial kits, while intracellular lipid accumulation (assessed using Oil Red O staining), total triglyceride content (measured via triglyceride quantification kit), and protein and mRNA levels (measured via Western blot and real-time quantitative polymerase chain reaction, respectively) were used to assess sterol regulatory element-binding protein-1, fatty acid synthase, stearoyl-CoA desaturase-1, and proliferator-activated receptor-α expression levels. After p-coumaric acid targets were identified using network pharmacological analysis, cyclooxygenase-2 (COX-2) expression was assessed via Western blot and prostaglandin E2 accumulation was measured via enzyme-linked immunosorbent assay. Notably, p-coumaric acid increased the percentage of viable cells in PA-treated hepatocyte from 65.5±2.5% to 87.3±2.2%, reduced the intracellular lipid accumulation and promoted lipolysis and fatty acid β-oxidation; this protective effect may depend on inhibition of both PA-induced HepG2 cell COX-2 expression and PGE2 accumulation.