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  2. Advanced oxidation protein products induce catabolic effect through oxidant-dependent activation of NF-κ B pathway in human chondrocyte

Advanced oxidation protein products induce catabolic effect through oxidant-dependent activation of NF-κ B pathway in human chondrocyte

  • Int Immunopharmacol. 2016 Oct;39:149-157. doi: 10.1016/j.intimp.2016.07.018.
Wenbin Ye 1 Zhaoming Zhong 1 Siyuan Zhu 1 Shuai Zheng 1 Jun Xiao 2 Shaolian Song 3 Hui Yu 1 Qian Wu 1 Zhen Lin 1 Jianting Chen 4
Affiliations

Affiliations

  • 1 Department of Orthopaedic Spinal Surgery, Nanfang Hospital, Southern Medical University, China.
  • 2 Department of Orthopedic Joint Surgery, Nanfang Hospital, Southern Medical University, China.
  • 3 Department of Pharmacy, Nanfang Hospital, Southern Medical University, China.
  • 4 Department of Orthopaedic Spinal Surgery, Nanfang Hospital, Southern Medical University, China. Electronic address: chenjianting99@126.com.
Abstract

Advanced oxidation protein products (AOPPs) have been shown to participate in the progression of rheumatoid arthritis (RA). However, the effect of AOPPs accumulation on catabolic effect in human chondrocyte and the underlying mechanism(s) remain unclear. The present study demonstrated that AOPPs inhibited cell viability and glycosaminoglycan (GAG) production in human chondrocyte. Exposure of chondrocyte to AOPPs significantly increased the production of catabolic factors, such as cyclooxygenase-2 (COX-2), matrix metalloproteinase 3 (MMPs)-3 and MMP-13. AOPPs stimulation induced ROS generation and NF-κ B p65 phosphorylation, which could be inhibited by soluble receptor for advanced glycan end products (sRAGE), NADPH Oxidase Inhibitor (apocynin), ROS scavenger (N-acetyl-cysteine, NAC). Furthermore, NF-κ B inhibitor Bay11-7082 significantly reversed the AOPPs-induced expression of catabolic factors and phosphorylation of NF-κ B p65. Targeting AOPPs-triggered catabolic effect might be as a promising option for patients with RA.

Keywords

Advanced oxidation protein products (AOPPs); Catabolism; Chondrocytes; Oxidative; Rheumatoid arthritis; Stress.

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