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首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Caffeic acid protects against IL-1 beta-induced inflammatory responses and cartilage degradation in articular chondrocytes
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Caffeic acid protects against IL-1 beta-induced inflammatory responses and cartilage degradation in articular chondrocytes

机译:咖啡酸可保护IL-1β诱导的炎症反应和关节软骨细胞的软骨降解

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摘要

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-1 beta 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-1 beta in vivo organ culture of articular cartilage. Besides, the IL-1 beta induced increased production of inflammation factors such as iNOS and COX2 could be inhibited by CA. Additionally, CA could also suppress IL-1 beta induced expression of cartilage matrix catabolic enzymes such as ADAMTS5 and MMPs. Moreover, CA could prevent IL-1 beta induced degradation of Collagen II and aggrecan in chondrocytes. Furthermore, CA inhibited NF-kappa B activity and the activation of JNK pathway. This study reveals that CA inhibits IL-1 beta induced inflammation responses through suppression of NF-kappa B and MAPK related JNK signaling pathways. These results demonstrate that CA may provide new avenues for osteoarthritis treatment in future.
机译:骨关节炎(OA)是一种常见的关节疾病,具有软骨丧失和破坏。已经证实,炎症在骨关节炎的进展中发挥着重要作用。咖啡中常见的关键膳食营养素(CA),咖啡含量的关键膳食营养素在各种炎症疾病中表明了其抗炎性能。然而,Ca在骨关节炎中的影响仍然探讨。在这里,我们研究了CA对IL-1β诱导的炎症因子表达的影响以及大鼠软骨细胞中胶原II和蛋白的降解。 Ca阻止了IL-1β在体内软骨培养物中诱导的软骨损伤。此外,IL-1β诱导诱导的炎症因子的产生增加,例如INOS和COX2可以被CA抑制。另外,CA也可以抑制IL-1β诱导的软骨基质分解代谢酶如Adamts5和MMPS表达。此外,CA可以预防IL-1β在软骨细胞中诱导胶原蛋白II和EggCan的降解。此外,Ca抑制了NF-Kappa B活性和JNK途径的激活。该研究表明,CA通过抑制NF-Kappa B和MAPK相关的JNK信号传导途径来抑制IL-1β诱导的炎症反应。这些结果表明,CA可以在将来为骨关节炎治疗提供新的途径。

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  • 作者单位

    Huazhong Univ Sci &

    Technol Tongji Med Coll Tongji Hosp Dept Orthoped Wuhan 430030 Hubei;

    Huazhong Univ Sci &

    Technol Tongji Med Coll Tongji Hosp Dept Orthoped Wuhan 430030 Hubei;

    Huazhong Univ Sci &

    Technol Tongji Med Coll Tongji Hosp Dept Orthoped Wuhan 430030 Hubei;

    Huazhong Univ Sci &

    Technol Tongji Med Coll Tongji Hosp Dept Orthoped Wuhan 430030 Hubei;

    Huazhong Univ Sci &

    Technol Tongji Med Coll Tongji Hosp Dept Orthoped Wuhan 430030 Hubei;

    Huazhong Univ Sci &

    Technol Tongji Med Coll Tongji Hosp Dept Orthoped Wuhan 430030 Hubei;

    Huazhong Univ Sci &

    Technol Tongji Med Coll Tongji Hosp Dept Orthoped Wuhan 430030 Hubei;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 治疗学;
  • 关键词

    Osteoarthritis; Caffeic acid; MAPK; NF-kappa B; MMPs; ADAMTS5;

    机译:骨膜炎;咖啡因酸;MAPK;NF-OLIS;MAMPS;ADS5;

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