骨关节炎
MAPK/ERK通路
软骨
化学
阿达姆斯
软骨细胞
药理学
炎症
内分泌学
一氧化氮
激酶
分子生物学
内科学
基质金属蛋白酶
医学
病理
生物化学
体外
生物
解剖
金属蛋白酶
血栓反应素
替代医学
作者
Sungmin Moon,Seul Ah Lee,Seul Hee Han,Bo-Ram Park,Myung Suk Choi,Jae-Sung Kim,Su-Gwan Kim,Heung-Joong Kim,Hong Sung Chun,Do Kyung Kim,Chun Sung Kim
标识
DOI:10.1016/j.biopha.2017.10.130
摘要
Codium fragile (Suringar) Hariot has been used as a potential remedy in traditional medicine because of its anti-inflammatory and anti-oxidant effects. Osteoarthritis is a chronic progressive joint disease, characterized by complex mechanisms related to inflammation and degeneration of articular cartilage. In this study, we aimed to evaluate the cartilage protective effect of an aqueous extract of Codium fragile (AECF) using rat primary chondrocytes and the osteoarthritis animal model induced by destabilization of the medial meniscus (DMM). In vitro, rat primary cultured chondrocytes were pre-treated with AECF (0.5, 1, and 2 mg/mL) for 1 h and then incubated with interleukin-1β (10 ng/mL) for 24 h. Nitrite production was detected by the Griess reagent. Alteration of the protein levels of iNOS, MMP-13, ADAMTS-4, ADAMTS-5, mitogen-activated protein kinases (MAPKs), and nuclear factor-κB (NF-κB) was detected by western blotting. In vivo, osteoarthritis was induced by DMM of Sprague Dawley (SD) rats. The rats subjected to destabilization of the medial meniscus (DMM) surgery were orally administered with AECF (50, 100, and 200 mg/kg bodyweight) or distilled water for 8 w. The severity of cartilage lesions was evaluated by safranin O staining and the Osteoarthritis Research Society International (OARSI) score. These results demonstrated that AECF significantly inhibited nitrite production and inhibited the levels of iNOS, MMP-13, ADAMTS-4, and ADAMTS-5 in interleukin-1β-induced rat primary cultured chondrocytes. Moreover, AECF suppressed interleukin-1β-induced NF-κB activation in the nucleus and phosphorylation of ERK1/2 and JNK in the cytosol. In vivo, the cartilage lesions in AECF‐treated osteoarthritis rats exhibited less proteoglycan loss and lower OARSI scores. These results suggested that AECF is a potential therapeutic agent for the alleviation of osteoarthritis progression.
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