Study on effect of Curculiginis Rhizoma and its active ingredient on PXR-CYP3A of L02 cells in different states.
- Author:
Chun-Miao XUE
1
;
Bing ZHANG
2
;
Zhi-Jian LIN
2
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Line; Cytochrome P-450 CYP3A; metabolism; Gene Expression; drug effects; genetics; Glucosides; pharmacology; Humans; Male; Plant Extracts; chemistry; pharmacology; Rats; Rats, Sprague-Dawley; Receptors, Steroid; metabolism; Resorcinols; pharmacology; Rubiaceae; chemistry
- From: China Journal of Chinese Materia Medica 2013;38(19):3348-3352
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo define the effect of Curculiginis Rhizoma and its active ingredient orcinol glucoside on PXR-CYP3A of L02 cells in normal and deficiency-cold states, in order to lay a foundation for studies on the mechanism of efficacy expression differentiation of Curculiginis Rhizoma in different states.
METHODSerums of normal and deficiency-cold rats were adopted to culture L02 cells and induce cells in normal and deficiency-cold states. After aqueous extracts from Curculiginis Rhizoma and its active ingredient orcinol glucoside were used in cells in different states, PXR protain expression and CYP3A activity of L02 cells in normal and deficiency-cold states were observed.
RESULTMTT results showed that aqueous extracts from Curculiginis Rhizoma and orcinol glucoside could significantly enhance viability of L02 cells. Aqueous extracts from Curculiginis Rhizoma could significantly reduce PXR protein expression of L02 cells in normal state, while orcinol glucoside could significantly reduce CYP3A activity and PXR protein expression of L02 cells in normal state. Meanwhile, aqueous extracts from Curculiginis Rhizoma could significantly increase CYP3A activity and PXR protein expression of L02 cells in deficiency-cold state, while orcinol glucoside could significantly reduce CYP3A activity and increase PXR protein expression of L02 cells in deficiency-cold state.
CONCLUSIONCurculiginis Rhizoma can activate PXR and induce CYP3A activity of L02 cells in deficiency-cold state, but with no effect or even counteraction on PXR and its induced CYP3A of L02 cells in normal state.