Ginseng may beta cell destruction which contributes to its antidiabetic influence in type 1 diabetes.

Abstract

The effects of ginseng extracts (GE) and several ginsenosides on cytokine-induced apoptosis were evaluated. In pancreatic beta-cell line MIN6N8 cells, the inhibitory effect of GE was significantly observed at 25-100 microg/mL: an 86-100% decrease of cytoplasmic DNA fragments quantified by an ELISA. The inhibitory effect of red ginseng (RG) extract was greater than that of white ginseng (WG) extract (IC50, 3.633 vs 4.942 microg/mL). Screening of several known ginsenosides, which were present in ginseng extracts at 0.124-1.19% (w/w) by HPLC analysis, revealed that the ginsenosides were responsible for the inhibition of beta-cell apoptosis at 0.1-1.0 microg/mL. The molecular mechanism, by which GE inhibited beta-cell apoptosis, appeared to involve the reduction of nitric oxide (NO) and reactive oxygen species (ROS) production, inhibition on p53/p21 expression, and inhibition on cleavage of caspases and poly(ADP-ribose) polymerase (PARP). This study suggests that ginseng may inhibit cytokine-induced apoptosis in beta-cells and, thus, may contribute via this action to the antidiabetic influence in type 1 diabetes.