Ginsenoside Rb1 prevents high glucose-induced Schwann cell injury through the mitochondrial apoptosis pathway

OBJECTIVE: To investigate the effects of ginsenoside Rb1 on high glucose-induced neurotoxicity and the underlying molecular mechanism in primary cultured Schwann cells (SCs). METHODS: Cultured SCs were divided into six groups that received (a) normal glucose, (b) osmotic control, (c) high glucose, (d) high glucose plus 1 ginsenoside Rb1, (e) high glucose plus 10 mu M ginsenoside Rb1, or (f) high glucose plus 100 mu M alpha lipoic acid (ALA). Intracellular reactive oxygen species (ROS) generation and mitochondrial trans membrane potential (Delta psi m) were detected by flow cytometric analyses. Apoptosis was confirmed by the annexin V-FITC/propidium iodide (P1) method, and the concentration of 8-hydroxy-2-deoxy guanosine (8-OHdG) was detected by an enzyme -linked immunosorbent assay. Western blotting was performed to analyze the expression levels of important transcription factors such as cytochrome c, bcl-2, bax, activated caspase-3, and activated poly (ADP-ribose) polymerase (PARP). RESULTS: Ginsenoside Rb1 inhibited high glucose -induced oxidative stress by decreasing ROS and 8-OHdG levels as well as mitochondrial depolarization in SCs. 3-(4,5)-dimethylthiahiazo(-z-y1)-3, 5-di-phenytetrazoliumromide and annexin V-FITC/PI assays showed that incubating SCs with high glucose decreased cell viability and increased the number of apoptotic cells, whereas treatment with ginsenoside Rb1 protected SCs against high glucose -induced cell damage. Furthermore, ginsenoside Rb1 down-regulated the expression of high glucose-induced bax and cytochrome c release but up-regulated bcl-2 expression. In addition, ginsenoside Rb1 attenuated high glucose-induced activation of caspase-3 and minimized cleavage of PARP in SCs. CONCLUSION: These results suggest that ginsenoside Rb1 antagonizes high glucose-induced oxidative stress and activation of the mitochondria! apoptosis pathway in SCs. (C) 2017 JTCM. All rights reserved.