Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.
Biomed Pharmacother. 2018 Nov;107:433-439. doi: 10.1016/j.biopha.2018.07.161. Epub 2018 Aug 10.
Osteoarthritis (OA) is a common articular disease that features cartilage loss and destruction. It has been confirmed that inflammation plays major roles in the progression of osteoarthritis. Caffeic acid (CA), a key dietary nutrient commonly found in coffee, has shown its anti-inflammatory properties in various inflammation diseases. However, the effects of CA in osteoarthritis remain explored. Here we investigated the effects of CA on IL-1β induced increased expression of inflammatory factors as well as the degradation of Collagen II and aggrecan in rat chondrocytes. CA prevented the cartilage damage induced by IL-1β in vivo organ culture of articular cartilage. Besides, the IL-1β induced increased production of inflammation factors such as iNOS and COX2 could be inhibited by CA. Additionally, CA could also suppress IL-1β induced expression of cartilage matrix catabolic enzymes such as ADAMTS5 and MMPs. Moreover, CA could prevent IL-1β induced degradation of Collagen II and aggrecan in chondrocytes. Furthermore, CA inhibited NF-κB activity and the activation of JNK pathway. This study reveals that CA inhibits IL-1β induced inflammation responses through suppression of NF-κB and MAPK related JNK signaling pathways. These results demonstrate that CA may provide new avenues for osteoarthritis treatment in future.
骨关节炎(OA)是一种常见的关节疾病,其特征是软骨丧失和破坏。已经证实炎症在骨关节炎的进展中起主要作用。咖啡酸(CA)是一种常见于咖啡中的关键膳食营养素,已在各种炎症性疾病中显示出其抗炎特性。然而,CA 在骨关节炎中的作用仍在探索中。在这里,我们研究了 CA 对 IL-1β诱导的炎症因子表达增加以及软骨细胞中 Collagen II 和 aggrecan 降解的影响。CA 可预防 IL-1β诱导的关节软骨体内器官培养中的软骨损伤。此外,CA 可抑制 IL-1β 诱导的炎症因子如 iNOS 和 COX2 的产生增加。此外,CA 还可以抑制 IL-1β 诱导的软骨基质分解代谢酶如 ADAMTS5 和 MMPs 的表达。此外,CA 可防止 IL-1β 诱导的软骨细胞中 Collagen II 和 aggrecan 的降解。此外,CA 抑制 NF-κB 活性和 JNK 信号通路的激活。这项研究表明,CA 通过抑制 NF-κB 和 MAPK 相关的 JNK 信号通路抑制 IL-1β 诱导的炎症反应。这些结果表明,CA 可能为未来的骨关节炎治疗提供新途径。