Metformin prevents methylglyoxal-induced apoptosis of mouse Schwann cells
- Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya (Japan)
- Department of Cellular Biology and Anatomy, School Medical College of Georgia, Augusta, GA (United States)
- Department of Internal Medicine, School of Denistry, Aichi Gakuin University, Nagoya (Japan)
- Department of Molecular Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Tokyo (Japan)
- Division of Endocrinology, Metabolism and Diabetology, Department of Internal Medicine, Aichi Medical University, Aichi (Japan)
- Department of Metabolic Medicine, Nagoya University School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550 (Japan)
Methylglyoxal (MG) is involved in the pathogenesis of diabetic complications via the formation of advanced glycation end products (AGEs) and reactive oxygen species (ROS). To clarify whether the antidiabetic drug metformin prevents Schwann cell damage induced by MG, we cultured mouse Schwann cells in the presence of MG and metformin. Cell apoptosis was evaluated using Hoechst 33342 nuclear staining, caspase-3 activity, and c-Jun-N-terminal kinase (JNK) phosphorylation. Intracellular ROS formation was determined by flow cytometry, and AMP-activated kinase (AMPK) phosphorylation was also examined. MG treatment resulted in blunted cell proliferation, an increase in the number of apoptotic cells, and the activation of caspase-3 and JNK along with enhanced intracellular ROS formation. All of these changes were significantly inhibited by metformin. No significant activation of AMPK by MG or metformin was observed. Taken together, metformin likely prevents MG-induced apoptotic signals in mouse Schwann cells by inhibiting the formation of AGEs and ROS.
- OSTI ID:
- 20991359
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 357, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2007.03.140; PII: S0006-291X(07)00632-8; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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