Exogenous pyruvate protects IMS32 Schwann cells from impairing the maturation process under hyperglycemia.

Peripheral neuropathy is a chronic common complication of diabetes mellitus. Continuous hyperglycemia induces metabolic disturbances and elicits oxidative stress. However, the impact of hyperglycemia on the maturation of Schwann cells is not fully understood. Therefore, we examined whether hyperglycemia affects the maturation process of IMS32 Schwann cells treated with forskolin, a Schwann cell maturation enhancer, using promoter assays and immunoblotting of Schwann cell markers such as MBP, CNPase, and GFAP. IMS32 cells exposed to high-glucose conditions showed decreased expression of these markers. Exogenous pyruvate plays a crucial role in maintaining glucose metabolism and reducing oxidative stress under hyperglycemic conditions. These decreases were prevented by pyruvate supplementation. Pyruvate treatment also prevented IMS32 cells from producing reactive oxygen species and from impairing mitochondrial membrane potential. These results indicate that hyperglycemia impairs Schwann cell maturation accompanied by mitochondrial dysfunction and oxidative stress, contributing to the development and progression of diabetic peripheral neuropathy.