The mechanism of ginsenosides Rg1 and Rb1 promoting glutamic acid release from PC12 cells.
- Author:
Jian-Fei XUE
1
;
Jin-Feng HU
;
Zhi-Jun LIU
;
Hong CHEN
;
Jun-Tian ZHANG
;
Nai-Hong CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Cyclic AMP-Dependent Protein Kinases; physiology; Fluorescent Antibody Technique; Ginsenosides; pharmacology; Glutamic Acid; secretion; Isoquinolines; pharmacology; Neurotransmitter Agents; secretion; PC12 Cells; Phosphorylation; Rats; Sulfonamides; pharmacology; Synapsins; metabolism
- From: Acta Pharmaceutica Sinica 2006;41(12):1141-1145
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the mechanism of ginsenosides Rg1 and Rb1 promoting glutamic acid release from PC12 cells.
METHODSThe amount of glutamic acid released from PC12 cells was measured by high performance liquid chromatography (HPLC). The effect of Rg1 and Rb1 on the phosphorylation of synapsins was detected with immunofluorescent staining and Western blotting.
RESULTSBoth Rg1 (10 micromol x L(-1)) and Rb1 (10 micromol x L(-1)) increased glutamic acid release from PC12 cells. The release of glutamic acid was decreased by pre-incubating with the PKA inhibitor H89. H89 inhibited the release of glutamic acid induced by Rb1, but had no effect on the release of glutamic acid induced by Rg1. Moreover, Rb1 enhanced the phosphorylation of synapsins via PKA pathway, Rg1 was out of touch with this.
CONCLUSIONRb1 may promote release of neurotransmitters by increasing the phosphorylation of synapsins via PKA pathway, whereas the up-regulation of neurotransmitters release induced by Rg1 is independent of the phosphorylation of synapsins.
