Butenolide induces apoptosis of cultured chondrocytes: study of its mechanism.
- Author:
Shi-jie WANG
1
;
Xiong GUO
;
Yin-gang ZHANG
;
Feng-ling REN
;
Shuang-qing PENG
;
Jun-ling CAO
;
Zhong-li SHI
;
Zeng-tie ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: 4-Butyrolactone; analogs & derivatives; pharmacology; Apoptosis; drug effects; Cells, Cultured; Chondrocytes; drug effects; Humans; In Situ Nick-End Labeling; Proto-Oncogene Proteins c-bcl-2; metabolism; Selenium; pharmacology; bcl-2-Associated X Protein; metabolism
- From: Journal of Southern Medical University 2007;27(4):414-417
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe cell apoptosis and Bcl-2 and Bax expression changes of chondrocytes induced by butenolide (BUT) and the inhibitory effect of selenium against BUT-induced chondrcyte apoptosis, to gain insights into the mechanism by which BUT induces chondrcyte apoptosis.
METHODSCartilage tissue reestablished from human fetal articular chondrocytes in vitro were treated with BUT at the concentrations of 0.1, 1.0 and 5.0 microg/ml and with the protective factor selenium. TUNEL method was used to detect chondrocyte apoptosis, which was quantified by flow cytometry. Immunohitochemistry was performed to analyze the expression of Bcl-2 and Bax in the reestablished cartilage tissue.
RESULTSBUT exposure induced chondrocyte apoptosis, and the apoptosis rate increased with the concentration increment of BUT from 0 to 1.0 mg/ml, resulting also increased positive expression rate of Bcl-2 and Bax(P<0.05). The apoptosis rate of chondrocytes in BUT+ selenium group was significantly lower than that of BUT groups (P<0.05), as was the positivity rate of Bcl-2 and Bax expression (P<0.05).
CONCLUSIONBUT induces chondrocyte apoptosis in positive relation with BUT concentration (from 0 to 1.0 mg/ml) and causes increased expressions of Bcl-2 and Bax. Selenium can inhibit the chondrocyte apoptosis induced by BUT.