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

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

Oncotarget (2017-09-28)
Qi Sun, Gaoyi Wu, Hang Chen, Lei Chen, Hongyu Chen, Guoxiong Zhu, Huaqiang Zhao
ANOTACE

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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Sigma-Aldrich
Anti-SOX9 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution