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Cultured Schwann cells were treated with 5.6 mM and 50 mM glucose alternating every 8 hours to simulate intermittent high glucose. The present study analyzed the neuroprotective effects of 1, 10 and 100 μM ginsenoside Rb1 on oxidative damage and apoptosis in Schwann cells induced by intermittent high glucose. Flow cytometry demonstrated that ginsenoside Rb1 reduced intermittent high glucose-mediated reactive oxygen species production. Enzyme linked immunosorbent assay showed that 8-hydroxy-2-deoxy guanosine levels in Schwann cells decreased following ginsenoside Rb1 treatment. Quantitative real-time reverse transcription-PCR and western blot assay results revealed that ginsenoside Rb1 inhibited intermittent high glucose-upregulated Bax expression, but antagonized intermittent high glucose-downregulated Bcl-2 expression in Schwann cells. These effects were most pronounced with 100 μM ginsenoside Rb1. These results indicate that ginsenoside Rb1 inhibits intermittent high glucose-induced oxidative stress and apoptosis in Schwann cells.
Cultured Schwann cells were treated with 5.6 mM and 50 mM glucose alternating every 8 hours to simulate intermittent high glucose. The present studies analyzed the neuroprotective effects of 1, 10 and 100 μM ginsenoside Rb1 on oxidative damage and apoptosis in Schwann cells induced by intermittent high glucose. Flow cytometry demonstrated that ginsenoside Rb1 reduced intermittent high glucose-mediated reactive oxygen species production. Enzyme linked immunosorbent assay showed that 8-hydroxy-2-deoxy guanosine levels in Schwann cells decreased following ginsenoside Rb1 treatment. Quantitative real-time reverse transcription- PCR and western blot assay results revealed that ginsenoside Rb1 inhibited intermittent high glucose-upregulated Bax expression, but antagonized intermittent high glucose-downregulated Bcl-2 expression in Schwann cells. These effects were most pronounced with 100 μM ginsenoside Rb1. These results indicate that ginsenoside Rb1 inhibits intermittent high glucose-induce d oxidative stress and apoptosis in Schwann cells.