Polyenylphosphatidylcholine alleviates palmitic acid-induced apoptosis in HepG2 cells via inhibiting endoplasmic reticulum stress

Polyenylphosphatidylcholine (PPC) can reduce hyperlipidemia, relieve arteriosclerosis and decrease triglyceride. The aim of the present study was to investigate whether polyenylphosphatidylcholine (PPC) could alleviate apoptosis induced by palmitic acid (PA), and explore the possible molecular mechanisms in HepG2 cells. In this study, MTT assay was performed to identify the cell viability after PA (50, 100, 150 and 200 mu mol/L) treatment for 24 h in HepG2 cells. The cell viability was significantly decreased by PA treatment in a dose dependent manner. Flow cytometry confirmed that co-incubation of PPC reduced PA-induced apoptosis. Moreover, the secretion level of tumor necrosis factor-alpha (TNF-alpha) was conspicuously reduced after PPC treatment using enzyme-linked immunosorbent assay (ELISA). We observed that treatment of the cells with PA resulted in activation of Endoplasmic Reticulum Stress (ERS) associated proteins including glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP). Western blot and real-time polymerase chain reaction (RT-PCR) confirmed that the expression levels of Bcl2 associated X protein (Bax) and B cell lymphoma-2 (Bcl-2) were significantly regulated and the expression levels of GRP78 and CHOP were dramatically decreased by co-incubation of PPC. These results suggested that PPC could alleviate cell apoptosis and reduce the ERS-related proteins expressions after cells pre-treatment with PA, which showed that ERS might play an important role in cell apoptosis caused by PA.