BACKGROUNDA number of studies have shown that oxidative stress and mitochondrial involvement are major triggering factors in the development of neurodegenerative diseases. Cobalt chloride (CoCl(2))-induced cell death in PC12 cells may serve a simple and convenient in vitro model of hypoxia-induced neuronal cytotoxicity. To explore the effect of geniposide on CoCl(2) which induced cytotoxicity and mitochondrial function in rat pheochromocytoma PC12 cells, we analyzed the influence of geniposide on the expression of apoptosis-related proteins.

METHODSPC12 cells and RNAi PC12 cells were treated with 0, 12.5, 25, 50, 100 micromol/L geniposide for 12 hours and then exposure to 400 micromol/L CoCl(2) for 12 hours. Cell viability, cell morphology, and expression of Bcl-2, Bax, P53 and caspase-9 were determined using Western blotting.

RESULTSPretreatment with geniposide markedly improved the cells viability and morphology, decreased the expression of Bax, P53 and caspase-9, and increased the expression of Bcl-2 in PC12 cells challenged by CoCl(2)2. However, in the RNAi PC12 cells, geniposide had no significant effect on the expression of these proteins.

CONCLUSIONGeniposide protects PC12 cells from CoCl(2) involved in mitochondrial mediated apoptosis, and GLP-1R might play a critical role in the neuroprotection of geniposide in PC12 cells.