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咖啡酸可预防白介素-1β诱导的软骨细胞炎症反应和软骨降解。

Caffeic acid protects against IL-1β-induced inflammatory responses and cartilage degradation in articular chondrocytes.

机构信息

Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.

出版信息

Biomed Pharmacother. 2018 Nov;107:433-439. doi: 10.1016/j.biopha.2018.07.161. Epub 2018 Aug 10.

Abstract

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.

摘要

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。

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