Oridonin induced U937 cell apoptosis through ERK pathway.
- Author:
Yan-qiu LIU
1
;
Song YOU
;
Shin-ichi TASHIRO
;
Satoshi ONODERA
;
Takashi IKEJIMA
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Proliferation; drug effects; DNA Fragmentation; drug effects; Diterpenes; administration & dosage; isolation & purification; pharmacology; Diterpenes, Kaurane; administration & dosage; isolation & purification; pharmacology; Dose-Response Relationship, Drug; Extracellular Signal-Regulated MAP Kinases; antagonists & inhibitors; metabolism; Flavonoids; pharmacology; Humans; Isodon; chemistry; Phosphorylation; Plants, Medicinal; chemistry; U937 Cells; bcl-2-Associated X Protein; metabolism; bcl-X Protein; metabolism
- From: China Journal of Chinese Materia Medica 2005;30(23):1856-1859
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the mechanisms of oridonin-induced U937 cell apoptosis, and to examine the role of ERK MAPK.
METHODMTT, Hoechst 33258 staining, DNA agarose gel electrophoresis and Western blot analysis were used.
RESULTOridonin inhibited U937 cell growth in a time- and dose-dependent manner. Apoptotic bodies were found with Hoechst 33258 staining after treatment with 27 micromol x L(-1) oridonin. Simultaneously, ERK phosphorylation was significant. ERK inhibitor PD98059 partially blocked the growth-inhibitory effect as well as DNA fragmentation. The expression of antiapoptotic mitochondrial protein Bcl-XL decreased time-dependently, and that of proapoptotic protein Bax increased. However, PD98059 reversed the effect of oridonin on Bcl-XL and Bax.
CONCLUSIONOridonin induces U937 cell apoptosis through activation of ERK and alteration of the ratio of Bax/Bcl-XL.
