Oncotarget

Research Papers:

Hyperbaric oxygen protects type II collagen in interleukin-1β-induced mandibular condylar chondrocyte via inhibiting the JNK/c-Jun signaling pathway

Qi Sun, Gaoyi Wu, Hang Chen, Lei Chen, Hongyu Chen, Guoxiong Zhu and Huaqiang Zhao _

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Oncotarget. 2017; 8:60312-60323. https://doi.org/10.18632/oncotarget.19294

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Abstract

Qi Sun1,2,*, Gaoyi Wu3,*, Hang Chen1,2, Lei Chen1,2, Hongyu Chen1,2, Guoxiong Zhu3 and Huaqiang Zhao1,2,4

1School of Stomatology, Shandong University, Jinan City, Shandong Province, China

2Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan City, Shandong Province, China

3Department of Stomatology, Jinan Military General Hospital, Jinan City, Shandong Province, China

4Present address: Department of Oral and Maxillofacial Surgery, School of Stomatology, Shandong University, Jinan City, Shandong Province, China

*These authors have contributed equally to this work

Correspondence to:

Huaqiang Zhao, email: [email protected]

Keywords: hyperbaric oxygen, IL-1β, JNK, COL2, Sox-9

Received: April 07, 2017    Accepted: June 05, 2017    Published: July 17, 2017

ABSTRACT

The aim of this study was to explore the mechanisms of Hyperbaric oxygen (HBO) protective on interleukin-1β (IL-1β) induced rat’s mandibular condylar chondrocytes. Chondrocytes were exposure to Hyperbaric oxygen after induced inflammatory by IL-1β. After that, the expression of p-JNK and c-Jun was increased significantly, while the Sox-9 was decreased significantly, Immunofluorescence results showed that the expression of p-JNK and p-c-Jun were decreased while the expression of Sox-9 and COL2 were increased in chondrocytes treated with IL-1β and selective JNK inhibitor. Hyperbaric oxygen might plays similar roles with the JNK-specific inhibitor SP600125, inducing the increase of Sox-9 and COL2 expression. On the whole, IL-1β induced inflammatory in chondrocytes by activating the JNK/c-Jun signaling pathway and down-regulate the expression of Sox-9 and COL2. However, Hyperbaric oxygen can inhibits IL-1β induced inflammatory response in chondrocytes though block the JNK/c-Jun signaling pathway and up-regulate the expression of Sox-9 and COL2.


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