Oncotarget

Research Papers:

Gallic acid inhibits the release of ADAMTS4 in nucleus pulposus cells by inhibiting p65 phosphorylation and acetylation of the NF-κB signaling pathway

Yao Huang, Jian Chen, Tao Jiang, Zheng Zhou, Bin Lv, Guoyong Yin _ and Jin Fan

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Oncotarget. 2017; 8:47665-47674. https://doi.org/10.18632/oncotarget.17509

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Abstract

Yao Huang1,*, Jian Chen1,*, Tao Jiang1,*, Zheng Zhou1, Bin Lv1, Guoyong Yin1 and Jin Fan1

1Department of Orthopaedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210000, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Guoyong Yin, email: guoyong_yin@sina.com

Jin Fan, email: fanjin@njmu.edu.cn

Keywords: GA, ADAMTS4, NF-κB, p65, degeneration

Received: March 17, 2017     Accepted: March 30, 2017     Published: April 28, 2017

ABSTRACT

This study investigated the inhibitory effect of gallic acid (GA) on the release of A Disintegrin and Metalloproteinase with Thrombospondin motifs 4 (ADAMTS4) through the regulation of the NF-κB signaling pathway, which is closely related to the matrix metalloproteinases in nucleus pulposus cells. Different concentrations of GA were added to TNF-α-induced human nucleus pulposus cells (hNPCs) and intervertebral disc degeneration rat model. ADAMTS-4 expression increased both in the TNF-α-induced nucleus pulposus cells and intervertebral disc degeneration rat model. By contrast, the release of ADAMTS-4 was reduced, and the TNF-α-induced apoptosis of nucleus pulposus cells was significantly inhibited after addition of GA at different concentrations. Further study found that the levels of phosphorylated p65 (p-p65) was increased and the classical NF-κB signal pathway was activated after the nucleus pulposus cells were stimulated by TNF-α. Meanwhile, GA suppressed the p65 phosphorylation and inceased p65 deacetylation levels. As a consequence, GA can decrease the expression of ADAMTS-4 in nucleus pulposus cells by regulating the phosphorylation and acetylation of p65 in NF-κB signaling pathways.


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