Lycium barbarum polysaccharide arbitrates palmitate-induced apoptosis in MC3T3-E1 cells through decreasing the activation of ERS-mediated apoptosis pathway

Palmitate (PA) has been identified to induce cell apoptosis in osteoblasts. The c-Jun NH2-teminal kinase (JNK) signaling pathway and endoplasmic reticulum stress (ERS) were found to be important contributors. Therefore, natural or synthetic agents may antagonize PA-induced apoptosis in osteoblasts, and demonstrate the potential application to reverse osteoporosis. The present study demonstrated that the Lycium barbarum polysaccharide (LBP) is as a major active ingredient of Lycium barbarum and that it can reduce the fatty acid toxicity of PA. Furthermore, this study attempted to elucidate the underlying molecular mechanisms of LBP. Firstly, it was demonstrated via a Cell Counting Kit-8 assay, that LBP could significantly increase the viability of MC3T3-E1 cells in a dose-dependent manner. Flow cytometric analysis indicated that LBP inhibits PA-induced apoptosis in osteoblastic cells. Reverse transcription-quantitative polymerase chain reaction and western blotting results showed that the expression levels of glucose-regulated protein 78, C/EBP homologous protein and cysteinyl asparate specific proteinase-3/-9/-12, were increased in MC3T3-E1 cells following PA treatment. The treatment of the cells with PA resulted in an activation of the ERS and the JNK signaling pathway. These pathways were effectively suppressed by co-incubation with LBP. Taken together, PA may cause ERS, in cell apoptosis, and it may further activate the JNK signaling pathway. LBP reversed PA-induced apoptosis in MC3T3-E1 cells through inhibition of the activation of the ERS-mediated JNK signaling pathway.