Butenolide induces apoptosis of cultured chondrocytes: study of its mechanism / 南方医科大学学报
Journal of Southern Medical University
; (12): 414-417, 2007.
Article
in Zh
| WPRIM
| ID: wpr-268119
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>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.</p>
Full text:
1
Index:
WPRIM
Main subject:
Pharmacology
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Selenium
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4-Butyrolactone
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Cells, Cultured
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Apoptosis
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Proto-Oncogene Proteins c-bcl-2
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Chondrocytes
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In Situ Nick-End Labeling
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Bcl-2-Associated X Protein
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Metabolism
Limits:
Humans
Language:
Zh
Journal:
Journal of Southern Medical University
Year:
2007
Type:
Article