Objective: To investigate the mechanism and inhibitory effects of salvianolic acid B (Sal B) on the intermittent high glucose (IHG)-induced Schwann cells (SCs) injury in vitro. Method: SCs were primarily cultured and were divided into various groups

such as normal

high glucose(HG)

IHG

osmotic controls

with IHG in the presence of 25

50

100 μmol · L-1 Sal B for 48 hrs. Apoptosis

intracellular reactive oxygen species(ROS) generation and mitochondrial transmembrane potential were detected by flow cytometry analysis. The concentration of 8-hydroxy-2-deoxy guanosine (8-OHdG) was detected by enzyme-linked immune sorbent assay(ELISA). Quantitative real-time reverse transcriptase PCR was performed to analyze the expression levels of B cell lymphoma/leukemia-2(Bcl-2) and Bcl-2 associated x protein(Bax) .Western blot were performed to analyze the expression levels of Bcl-2

Bax

Caspase-3 and PARP. Result: The relative levels of intracellular ROS and the percentages of depolarized cells in the IHG group was significantly increased than those in the control and HG group(P<0.05

P<0.01). The concentrations of 8-OHdG showed a marked increase in SCs that were exposed to HG group compared with normal glucose exposure and further increased under IHG conditions(P<0.01). Compared to the normal and HG group

treatment with IHG down-regulated the Bcl-2 expression of protein and mRNA(P<0.01)

but up-regulated the Bax expression of protein and mRNA(P<0.01). In addition

treatment with IHG increased the activation of Caspase-3 and the cleavage of PARP in SCs(P<0.01). The percentages of apoptotic cells was increased exposed to HG and substantially more in cells exposed to the IHG(P<0.01). Treatment with Sal B inhibited the IHG-induced oxidative stress by reducing ROS production

8-OHdG levels

mitochondrial depolarization

and apoptosis in SCs(P<0.01). Furthermore

treatment with Sal B mitigated the IHG-mediated up-regulation of Bax expression and down-regulation of Bcl-2 expression in SCs(P<0.05

P<0.01). In addition

treatment with Sal B attenuated the IHG-induced activation of Caspase-3 and minimized the cleavage of PARP (P<0.01). Conclusion: The cytotoxic effect of IHG may be significantly more potent than that of HG and Sal B antagonized the IHG-induced injury of SCs.