首页> 美国卫生研究院文献>Oncotarget >Hyperbaric oxygen protects type II collagen in interleukin-1β-induced mandibular condylar chondrocyte via inhibiting the JNK/c-Jun signaling pathway
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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

机译:高压氧通过抑制JNK / c-Jun信号通路保护白介素1β诱导的下颌con突软骨细胞中的II型胶原

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摘要

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.
机译:这项研究的目的是探讨高压氧(HBO)对白介素1β(IL-1β)诱导的大鼠下颌con突软骨细胞保护的机制。 IL-1β诱导炎症后,软骨细胞暴露于高压氧。之后,p-JNK和c-Jun的表达显着增加,而Sox-9的表达显着下降,免疫荧光结果显示p-JNK和pc-Jun的表达降低,而Sox-9和c-Jun的表达下降。 IL-1β和选择性JNK抑制剂处理的软骨细胞中COL2升高。高压氧可能与JNK特异性抑制剂SP600125发挥相似的作用,从而导致Sox-9和COL2表达增加。总体而言,IL-1β通过激活JNK / c-Jun信号通路并下调Sox-9和COL2的表达诱导软骨细胞炎症。然而,高压氧虽然可以阻断JNK / c-Jun信号通路并上调Sox-9和COL2的表达,但仍可以抑制软骨细胞中IL-1β诱导的炎症反应。

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