THE REDUCED COENZYME NICOTINAMIDE ADENINE-DINUCLEOTIDE (NADH) RESCUESPC12 CELLS FROM APOPTOSIS

In order to investigate whether NADH can trigger proliferation activit y of nerve cells and rescue nerve cells from apoptotic damage induced by cisplatin the changes of the cell proliferation genes (c-myc, c-erb B-2), apoptosis inhibition genes (bcl-2, P53), cell apoptosis gene (c- fos) and cyclin proteins (cyclin A1, B1, and D1) on PC12 cells damaged by cisplatin were analyzed by cycotoxicity test and flow cytometry an alysis. The results show that after incubation with cisplatin for 12 h ours, the apoptotic rate of PC12 cells is 82.4%. The cells were mainly arrested in the G1 phase and showed an higher expression of cyclin D1 . The amount of P53, Bcl-2, c-erbB-2, c-myc, cyclin A, cyclin B1 expre ssed on the PC12 cells damaged by cisplatin were round to be down-regu lated to 52.2%, 60.8%, 21.9%, 90.7%, 40.9%, and 58.5% respectively. Fl ow cytometry analysis confirmed that after incubated with NADH for 48 hours, the amounts of P53, Bcl-2 and cyclin B1 expressed on the cells damaged by cisplatin were significantly rescued and upregulated. The e xpression of p53 tumor suppressor protein was downregulated by 59.6% i n comparison with the goup incubated with medium alone. However, the e xpression of c-myc and c-erbB-2 oncogene proteins on the PC12 cells di d not show a significant increase in the group treated with NADH. It i s suggested that NADH can not only promote survival and differentiatio n, but also rescue the PC12 cells from apoptotic damage by upregulatio n of P53 and Bcl-2 and downregulation of cyclinD1, c-fos expressed on the PC12 cells.