Abstract
Diabetic peripheral neuropathy (DPN) is one of the most common and debilitating microvascular complications of diabetes, and there is no effective therapy for the prevention or treatment of DPN. Oxidative stress triggers several pathways of injury and may be the unifying factor of hyperglycemia. The aim of this study was to investigate protective effect of Salvianolic acid B (Sal B) on the high glucose (HG)-induced oxidative stress-induced mitochondrial pathway activation and Schwann cells (SCs) apoptosis in vitro. We found that Sal B inhibited the HG-induced oxidative stress by reducing ROS and 8-hydroxy-2-deoxy Guanosine (8-OHdG) production, and mitochondrial depolarization and apoptosis in SCs in a dose-dependent manner. Furthermore, Sal B down-regulated the HG-mediated Bax expression and AIF nuclear translocation and the release of cytochrome c, but up-regulated the HG-induced BcL-2 expression in SCs. In addition, Sal B attenuated the HG-induced activation of caspase 3 and 9 and minimized the cleavage of PARP in SCs. Our results indicated that Sal B antagonized the HG-induced oxidative stress, activation of the mitochondrial pathway and apoptosis in SCs.
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