Background: The study was performed to investigate whether ginseng has protective effect in an experimental mouse model of cyclosporine (CsA)-induced pancreatic injury.

Methods: Mice were treated with CsA (30 mg/kg/day, s.c.) and Korean red ginseng extract (0.2, 0.4 g/kg/day, P.O.) under 0.01% salt diet for 4 weeks. The effect of ginseng on CsA-induced pancreatic islet dysfunction was investigated by an intraperitoneal glucose tolerance test (IPGTT), serum insulin level, islet cell mass, macrophage infiltration, and apoptosis. Using in vitro model, we further examined the effect of ginseng in CsA-treated pancreatic Β-cells (INS-1). Oxidative stress was measured with concentration of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in serum, tissue sections, and culture media.

Results: Four weeks of CsA treatment increased blood glucose level, decreased insulin level, but ginseng co-treatment recovered CsA-induced hyperglycemia. Pancreatic islet mass also increased with ginseng treatment compared with CsA monotherapy. Pro-inflammatory molecules such as iNOS, cytokines, and apoptotic cell death also decreased with ginseng treatment. Consistently, in vitro study showed that addition of ginseng protected against CsA-induced cytotoxicity, inflammation, and apoptotic cell death proved by annexin V-binding assay. These changes from in vivo and in vitro were accompanied by decreased the level of 8-OHdG in serum, tissue, culture media during ginseng addition.

Conclusion: The results of our in vivo and in vitro study demonstrate that ginseng has protective effect against CsA-induced pancreatic injury via reducing oxidative stress.

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