Wang Shi-jie, Guo Xiong, Zhang Yin-gang, Ren Feng-ling, Peng Shuang-qing, Cao Jun-ling, Shi Zhong-li, Zhang Zeng-tie
Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing 100850, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2007 Apr;27(4):414-7.
To 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.
Cartilage 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.
BUT 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).
BUT 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.
观察丁烯内酯(BUT)诱导软骨细胞凋亡及Bcl-2和Bax表达的变化,以及硒对BUT诱导软骨细胞凋亡的抑制作用,以探讨BUT诱导软骨细胞凋亡的机制。
将体外培养的人胎儿关节软骨细胞重建的软骨组织分别用浓度为0.1、1.0和5.0μg/ml的BUT及保护性因子硒进行处理。采用TUNEL法检测软骨细胞凋亡,并通过流式细胞术进行定量分析。采用免疫组织化学法分析重建软骨组织中Bcl-2和Bax的表达。
BUT处理诱导软骨细胞凋亡,凋亡率随BUT浓度从0增加至1.0mg/ml而升高,同时Bcl-2和Bax的阳性表达率也升高(P<0.05)。BUT+硒组软骨细胞的凋亡率显著低于BUT各处理组(P<0.05),Bcl-2和Bax表达的阳性率也显著降低(P<0.05)。
BUT诱导软骨细胞凋亡,且与BUT浓度(0至1.0mg/ml)呈正相关,并导致Bcl-2和Bax表达增加。硒可抑制BUT诱导的软骨细胞凋亡。