title: Ginsenosides may reverse the dexamethasone-induced down-regulation of glucocorticoid receptor.
abstract: The effects of glucocorticoid (GC) hormones are mediated via an intracellular receptor, the glucocorticoid receptor (GR). It has been established that glucocorticoid down-regulate GR. Ginsenosides (GSS) from extract of Panax ginseng have demonstrated glucocorticoid-like activities in homeostasis and regulation of immunity, etc. We hypothesize that ginsenosides might mediate some of their actions by binding to the GR. The present study is aimed to determine whether GSS can act like a GC analog in the activation of glucocorticoid response element-luciferase activity in HL7702 cells. We found that GSS alone had no effect on the expression of reporter gene, but it enhanced dexamethasone (Dex)-induced transcription of reporter gene. To further explore the effects of GSS, we examined the influence of GSS on the gene and protein expression as well as hormone binding activity of GR by semi-quantitative RT-PCR, Western blot, and radioligand-binding assay, respectively. GSS partially reversed the Dex-induced decrease in GR expression and hormone binding activity with an optimal dose of 25 microg/ml, implicating a positive regulatory effect of GSS on GR expression and binding activity. Therefore, our result suggests that GSS may reverse partially the dexamethasone-induced down-regulation of glucocorticoid receptor.
authors.affiliation: Department of Chinese Traditional Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, China. lingchuangquan168@hotmail.com
authors.forename: Changquan
authors.initials: C
authors.lastname: Ling
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Zhu
authors.forename: Chen
authors.initials: C
authors.lastname: Zhang
authors.forename: Min
authors.initials: M
authors.lastname: Li
mesh_terms: D015153:Blotting, Western; D002460:Cell Line; D003907:Dexamethasone / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology*; D015536:Down-Regulation / Q000187:drug effects; D004357:Drug Synergism; D036145:Ginsenosides / Q000494:pharmacology*; D005938:Glucocorticoids / Q000378:metabolism; D006727:Hormone Antagonists / Q000494:pharmacology; D006801:Humans; D008156:Luciferases / Q000235:genetics; D008516:Medicine, Chinese Traditional; D015735:Mifepristone / Q000494:pharmacology; D012333:RNA, Messenger / Q000737:chemistry / Q000235:genetics; D011869:Radioligand Assay; D011965:Receptors, Glucocorticoid / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014158:Transcription, Genetic / Q000187:drug effects; D014162:Transfection
chemical_list: D036145:Ginsenosides; D005938:Glucocorticoids; D006727:Hormone Antagonists; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D003907:Dexamethasone; D008156:Luciferases