Ginseng (Panax ginseng C.A. Meyer) is widely used in Asian countries as a traditional medicine for the treatment of various diseases. It is known to have anti-inflammatory effects, although the mechanism is not clear. In this study, preventive effects of fermented ginseng (FG) against streptozotocin (STZ)-induced pancreatic β-cell death was assessed in RINm5F insulinoma cells. FG markedly inhibited the production of nitrite in a dose-dependent manner. The decrease in nitrite production was found to correlate with reduced inducible nitric oxide (iNOS) protein and mRNA levels. To characterize the anti-inflammatory mechanism of FG at the transcriptional level, we examined effects of FG on the activity of nuclear factor-κB (NF-κB). FG reduced a translocation of the NF-κB subunit and NF-κB-dependent transcriptional activity. FG blocked signaling upstream of NF-κB activation, such as degradation of inhibitor factor-κBα (IκBα ) and phosphorylations of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK). These results suggest that FG protects against STZ-induced pancreatic β-cell damage by downregulation of iNOS, cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α ) gene expressions by blocking NF-κB and mitogen-activated protein kinase activities.

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