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Melatonin protects against apoptotic and autophagic cell death in C2C12 murine myoblast cells

Chi Hyun Kim1, Kyung Hwan Kim, Yeong-Min Yoo

  • 1Department of Biomedical Engineering, College of Health Science, Yonsei University, Wonju, Gangwon-do, Korea.

Journal of Pineal Research
|December 9, 2010
PubMed

Insights

Melatonin protects C2C12 myoblast cells from cell death induced by nitric oxide or nutrient starvation. This antioxidant melatonin treatment enhances protective proteins like Bcl-2 and reduces cell death markers, preserving cell viability.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Apoptotic and autophagic cell death are critical cellular processes.
  • Nitric oxide (NO) and nutrient starvation can induce cell death in C2C12 murine myoblasts.
  • Melatonin's role in modulating these cell death pathways requires further investigation.

Purpose of the Study:

  • To investigate the inhibitory effects of melatonin on apoptotic and autophagic cell death in C2C12 cells.
  • To elucidate the molecular mechanisms underlying melatonin's protective actions.

Main Methods:

  • C2C12 murine myoblast cells were treated with S-nitroso-N-acetylpenicillamine (SNAP) as an NO donor or subjected to nutrient starvation.
  • Melatonin (100 μm) was administered to assess its protective effects.
  • Key proteins involved in apoptosis (Akt, Bad, Bcl-2, Bax) and autophagy (LC3-II), as well as antioxidant enzymes (catalase, Mn-SOD, Cu/Zn-SOD), were analyzed for expression levels.

Main Results:

  • Melatonin significantly attenuated NO-induced cell death by preventing decreased p-Akt expression and increasing p-Bad (Ser 136) expression.
  • Melatonin treatment upregulated Bcl-2 and downregulated Bax expression, while also elevating catalase and Mn-superoxide dismutase (SOD) levels.
  • Melatonin suppressed nutrient starvation-induced autophagic cell death, indicated by reduced LC3-II expression, with similar effects on Bcl-2, Bax, and SOD expression as observed in apoptosis.

Conclusions:

  • Melatonin confers protection against both apoptotic and autophagic cell death in C2C12 cells.
  • The protective mechanism involves a common pathway characterized by increased Bcl-2 and decreased Bax expression.
  • Melatonin's antioxidant properties, evidenced by altered SOD and catalase expression, contribute to its cytoprotective effects.

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