Melatonin protects against apoptotic and autophagic cell death in C2C12 murine myoblast cells
Article first published online: 8 DEC 2010
© 2010 The Authors. Journal of Pineal Research © 2010 John Wiley & Sons A/S
Journal of Pineal Research
Volume 50, Issue 3, pages 241–249, April 2011
How to Cite
Kim, C. H., Kim, K. H. and Yoo, Y.-M. (2011), Melatonin protects against apoptotic and autophagic cell death in C2C12 murine myoblast cells. Journal of Pineal Research, 50: 241–249. doi: 10.1111/j.1600-079X.2010.00833.x
- Issue published online: 11 MAR 2011
- Article first published online: 8 DEC 2010
- Received July 9, 2010; accepted October 19, 2010.
- C2C12 cells;
Abstract: In this study, we investigated whether or not melatonin inhibits apoptotic and autophagic cell death in C2C12 murine myoblast cells. Treatment of cells with S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, was shown to induce cell death, and treatment with melatonin (100 μm) significantly attenuated the occurrence of NO-induced cell death. Decreased p-Akt expression in response to NO was also arrested by melatonin. Under these conditions, p-Bad (Ser 136) expression increased with melatonin treatment prior to NO treatment. Treatment with Akt inhibitors (LY 294002, wortmannin) plus melatonin reduced p-Akt expression. Compared with NO treatment, Bcl-2 expression increased with melatonin treatment, while Bax expression was inhibited by melatonin treatment. Expression of catalase and Mn-superoxide dismutase (SOD) was elevated with melatonin treatment, whereas Cu/Zn-SOD expression decreased with melatonin, lower than NO treatment, respectively. Next, we investigated the question of whether or not melatonin may restrain autophagic cell death in C2C12 cells. Nutrient starvation induced a rise in expression of the microtubule-associated protein 1 light chain 3 (LC3)-II; however, melatonin treatment suppressed LC3-II expression by nutrient deprivation. Expression of Bcl-2, Bax, catalase, and Cu/Zn-SODs coincided with results of apoptotic cell death. Together, these results suggest that melatonin protects against apoptotic and autophagic cell death through the common pathway resulted in the increment of Bcl-2 expression and the reduction of Bax expression in C2C12 murine myoblast cells.