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.
Highlights
OA is the commonest joint disease that characterized by the progressive degeneration of articular cartilage and the destruction of joint [1]
The expression of p-c-Jun N-terminal kinase (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 type II collagen (COL2) were increased in chondrocytes treated with IL-1β and selective JNK inhibitor
The western blot analysis revealed that the expression of p-JNK and p-c-Jun was significantly increased while the expression of COL2 and Sox-9 was obviously decreased in the IL-1β treated groups in a dose dependent manner
Summary
OA is the commonest joint disease that characterized by the progressive degeneration of articular cartilage and the destruction of joint [1]. Vascular tissue was absent in normal articular cartilage in the hypoxia environment [2]. The degradation of the extracellular matrix (ECM) is a critical process in the development of osteoarthritis [5]. Temporomandibular joint osteoarthritis (TMJOA) is a degenerative joint disease characterized by the death of chondrocytes, the loss of cartilage ECM, and the subchondral bone resorption in its early stages, followed by abnormal reparative bone turnover [6]. Several studies have reported that TMJOA could occur the erosion of articular cartilage which predominantly resulting the imbalance between chondrocytecontrolled catabolic and anabolic processes [8, 9]
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