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KMID : 0869020100130020080
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Journal of Korean Orthopaedic Research Society
2010 Volume.13 No. 2 p.80 ~ p.87
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Glucocorticoid Mechanism of Inhibition of the Inflammatory Cells in Lumbar Intervertebral Disc Cells Stimulated by TNF-αProduction of Nuclear Factor-αB
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Oh In-Soo
Park Sang-Eun
Sohn Jong-Min
Chung Jun-Young
Kim Young-Yul
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Abstract
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Purpose: To analyze the action mechanism of NF-κB, IκB-αand effect of the Dexamethasone (DEXA) in mediating this inflammation, after stimulating cultured herniated intervertebral disc cells with TNF-α.
Materials and Methods: After cultured human intervertebral disc cells passaged three times, they were
divided into four groups: A control group (A), DEXA treatment group (B), TNF-αtreated group (C), TNF-α and DEXA were treated at the same time (D). IL-6 and IL-1βgene expression were measured with semi-quantitative RT-PCR. Western blot analysis was performed to measure protein expression of IκB-α in the above groups for 10 minutes, 1 hour, 2 hours. In addition, in order to explain the mechanism of NF-κB nuclear binding for each group, the nuclear amount of NF-κB binding in the nucleus is measured by EMSA .
Results: In RT-PCR, expression of IL-6 and IL-1βwas greatest in group C, followed by group D, group A. IκB-αexpression of the group treated with DEXA was not detected in Western blot results within 10 minutes. However, if stimulated by TNF-α, the DEXA was not inhibited of IκB-αconcentration. After 1 hour and 2 hours, IκB-αlevels were expressed by cells autonomously (autoregulatory induction). EMSA results expression levels in nuclear protein was maintained in accordance with protein expression.
Conclusions : Our study shows that DEXA inhibits the production of mediators such as inflammatory IL-6 and IL-1β, however, may not inhibit the transcription of NF-κB stimulated by TNF-α.
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KEYWORD
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Disc cell, NF-κB, IκB-α, IL-6, IL-1β, RT-PCR
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