Antioxidant and anti-inflammatory effects of Chinese propolis during palmitic acid-induced lipotoxicity in cultured hepatocytes

- Chinese propolis (CP) mitigate palmitic acid-induced lipotoxicity in hepatocytes.
- Polyphenolic compounds were analyzed in CP based on HPLC-DAD/Q-TOF-MS.
- CP helped restore the energy provision and prevented lipoapoptosis in hepatocytes.

Overload of hepatic palmitate, like palmitic acid (PA), is known as the key trigger for non-alcoholic fatty liver disease. Here, we investigated whether Chinese propolis (CP) would mitigate PA-induced lipotoxicity in hepatocytes. Total of 20 phenolic compounds were analysed in CP using HPLC-DAD/Q-TOF-MS. PA has significant cytotoxic effects on HepG2 and L02 hepatocytes, by decreasing cell viability and inducing LDH releases, which was rescued by CP pre-treatment. Lipoapoptosis was also found in HepG2 hepatocytes treated with PA and CP helped restore the energy provision and prevented cell apoptosis. After PA challenges, antioxidant effects of CP were also observed by boosting the HepG2 cellular total-antioxidant potentials, increasing superoxide dismutase level and up-regulating antioxidant/detoxicant gene expressions (GSTA1, TXNRD1, NQO-1, HO-1 and Nrf2). Notably, gene expressions of inflammatory cytokine, TNF-α and IL-8, were decreased by CP. Therefore, CP protects hepatocytes against PA-induced lipotoxicity by lowering biomarkers of apoptosis, oxidative stress and inflammation.