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KMID : 0545120190290020297
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Journal of Microbiology and Biotechnology
2019 Volume.29 No. 2 p.297 ~ p.303
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Dexamethasone Facilitates NF-κB Signal Pathway in TNF-α Stimulated Rotator Cuff Tenocytes
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Ji Jong-Hun
Kim Young-Yul
Patel Kaushal
Cho Nam-Joon
Park Sang-Eun
Ko Myung-Sup
Park Suk-Jae
Kim Jong-Ok
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Abstract
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Corticosteroids are commonly used for pain control in rotator cuff tear. Deregulated NF-κB activation is a hallmark of chronic inflammatory diseases and has been responsible for the pathogenesis of rotator cuff tear. The Dexamethasone(DEXA) is a synthetic corticosteroid. The purpose of this study was to examine the exact effect of dexamethasone on NF-κB signaling in rotator cuff tear. We measured NF-κB expression in four groups: control, TNF-α-treated, DEXA-treated, and combined treatment with TNF-α and DEXA. Tenocytes were isolated from patients with rotator cuff tears and pre-incubated with TNF-α (10 ng/ml), DEXA (1 μM), or both of them for 10 min, 1 h, and 2 h. Expression of p65, p50, and p52 in the nuclei and cytosol was analyzed by western blotting and immunofluorescence imaging using confocal microscopy. We also evaluated nucleus/cytosol (N/C) ratios of p65, p50, and p52. In our study, the combined treatment with DEXA and TNF-α showed increased N/C ratios of p65, p50, and p52 compared with those in the TNF-α group at all time points. Additionally, in the DEXA group, N/C ratios of p65, p50, and p52 gradually increased from 10 min to 2 h. In conclusion, DEXA promoted the nuclear localization of p65, p50, and p52, but was not effective in inhibiting the inflammatory response of TNF-α-stimulated rotator cuff tear.
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KEYWORD
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Rotator cuff, tenocytes, NF-kappa B, glucocorticoid, tumor necrosis factor-alpha
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