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Metformin prevents methylglyoxal-induced apoptosis of mouse Schwann cells
Kimiko Ota1, Jiro Nakamura, Weiguo Li
1Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Abstract:
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.
Insights
Metformin protects mouse Schwann cells from methylglyoxal (MG)-induced damage by reducing apoptosis and reactive oxygen species (ROS). This suggests metformin
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Methylglyoxal (MG) contributes to diabetic complications by forming advanced glycation end products (AGEs) and reactive oxygen species (ROS).
- Schwann cells are crucial for peripheral nerve function and are vulnerable to oxidative stress and glycation.
- Understanding protective mechanisms against MG-induced damage is vital for managing diabetic neuropathy.
Purpose of the Study:
- To investigate the protective effects of metformin against methylglyoxal (MG)-induced damage in mouse Schwann cells.
- To elucidate the molecular mechanisms underlying metformin's action in this context.
Main Methods:
- Mouse Schwann cells were cultured with MG and metformin.
- Apoptosis was assessed via nuclear staining, caspase-3 activity, and JNK phosphorylation.
- Intracellular ROS levels were measured using flow cytometry.
- AMP-activated kinase (AMPK) phosphorylation was examined.
Main Results:
- MG exposure led to reduced cell proliferation, increased apoptosis, and elevated caspase-3 activity and JNK phosphorylation.
- MG significantly increased intracellular ROS formation.
- Metformin treatment markedly inhibited MG-induced apoptosis, caspase-3 activation, JNK phosphorylation, and ROS production.
- Neither MG nor metformin significantly activated AMPK.
Conclusions:
- Metformin effectively prevents methylglyoxal (MG)-induced apoptotic cell death in mouse Schwann cells.
- The protective effect of metformin appears to be mediated by the inhibition of AGEs and ROS formation.
- Metformin's mechanism does not involve AMPK activation in this model.
