未折叠蛋白反应
切碎
细胞凋亡
内质网
MMP2型
化学
时间1
炎症
骨关节炎
促炎细胞因子
下调和上调
软骨
免疫印迹
标记法
药理学
医学
癌症研究
内科学
病理
生物化学
基因表达
解剖
替代医学
基因
作者
Yanghua Tang,Zhen‐shuang Yue,Wenjie Zheng,Hongfei Shen,Linru Zeng,Zhongqing Hu,Zhenfei Xiong
摘要
Abstract Osteoarthritis (OA) is a common bone and joint disease with a wild range of risk factors, which is associated with endoplasmic reticulum (ER) stress. The aim of our study was to discuss the possible mechanism of ER stress associated with OA in vivo and explore novel therapeutic method against OA. OA‐induced damages in cartilage tissues were evaluated by HE, Safranin O/fast green, and TUNEL staining. The inflammatory factors concentration and the expression of FAP, MMP2, MMP9, Bax, Bcl‐2, CHOP, and GRP78 were evaluated by ELISA, real‐time PCR, and Western blot analyses. As results, 4‐phenylbutyric acid (4‐PBA)‐treated OA cartilage tissues presented alleviated tissue damage with less apoptotic cells and cytokine production in comparison with advanced‐OA tissues. Downregulation of Bax/Bcl‐2, CHOP, GRP78, inflammatory factors, and reactive oxygen species generation, and the increase of MMP level detected after 4‐PBA treatment indicated an inhibitory effect of 4‐PBA on cell apoptosis, inflammatory response, and ER stress in OA. In conclusion, we indicate that ER stress causes cell apoptosis and inflammatory response, resulting in the tissue damage within OA. At the same time, 4‐PBA exhibited protective effect on cartilage cells against OA through the inhibition of ER stress.
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