Experimental study of ginsenosides in reversing the down-regulation of glucocorticoids on glucocorticoid receptor

Objective To observe the effect of ginsenosides (GS) on the action of glucocorticoid (GC) in down-regulating glucocorticoid receptor (GR), and to explore the mechanism. Methods The rat model with hepatic artery ligation (HAL) was established and treated with GS and dexamethasone (DEX). Serum corticosterone level, maximal GK binding capacity (GR Bmax), K and GR mRNA in liver cells were detected 12 h after HAL. Results The levels of corticosterone in GS group and model group were higher than those in GS + DEX group, DEX group and normal group (all P < 0.01). The levels of corticosterone in GS + DEX group and DEX group were higher than that of normal group (both P <0.01). Compared to model group, GR Bmax in GS group was higher (P < 0.05), GR Bmax in GS + DEX group was lower (P < 0.05), but higher than that of DEX group (P <0.01). The expression of GR mRNA in GS group was significantly higher than model group (P < 0.01), but GR mRNA expression in DEX group was lower than that in model group, normal group and GS + DEX group (P <0.01). Conclusion GS partially reverses the down-regulation of GC on GR Bmax and GR mRNA, but it has no effect on serum corticosterone level in the rat model with HAL. Key words: Ginsenosides;  Dexamethasone;  Glucocorticoid;  Receptor