首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Osteoarthritis Is a Low-Grade Inflammatory Disease: Obesity’s Involvement and Herbal Treatment
【24h】

Osteoarthritis Is a Low-Grade Inflammatory Disease: Obesity’s Involvement and Herbal Treatment

机译:骨关节炎是一种低级别的炎症性疾病:肥胖的参与和草药治疗

获取原文
获取外文期刊封面目录资料

摘要

Osteoarthritis (OA) is considered a major cause of disability around the globe. This handicapping disease causes important cartilage and bone alteration that is associated with serious pains and loss of joint function. Despite its frequent association with obesity, the aetiology of OA is not fully understood. In this review, the different aspects of OA and its correlation with obesity were analysed. Through examining different mechanisms by which obesity may trigger and/or exacerbate OA, we point out some relevant signalling pathways that may evolve as candidates for pharmacological drug development. As such, we also suggest a review of different herbal medicines (HMs) and their main compounds, which specifically interfere with the identified pathways. We have shown that obesity’s involvement in OA is not only limited to the mechanical weight exerted on the joints (mechanical hypothesis), but also induces an inflammatory state by different mechanisms, including increased leptin expression, compromised gut mucosa, and/or gut microbiota disruption. The main signalling pathways involved in OA inflammation, which are associated with obesity, are protein tyrosine phosphatase 1B (PTP1B) and TLR4 or DAP12. Moreover, we also underline the contamination of plant extracts with LPS as an important factor to consider when studying HM’s effects on articular cells. By summarizing recent publications, this review aims at highlighting newly established aspects of obesity involvement in OA other than the mechanical one.
机译:骨关节炎(OA)被认为是全球残疾的主要原因。这种障碍疾病导致重要的软骨和骨骼改变,与严重的痛苦和关节功能丧失相关。尽管它经常与肥胖症结合,但OA的​​乙型学不完全明白。在该评论中,分析了OA的不同方面及其与肥胖的相关性。通过检查肥胖可以触发和/或加剧OA的不同机制,我们指出了一些可能随着药物药物发育的候选者发展的一些相关信号通路。因此,我们还表明对不同草药(HMS)及其主要化合物的审查,该化合物特别干涉所识别的途径。我们已经表明,肥胖症的OA的参与不仅限于施加在关节上的机械重量(机械假设),而且还通过不同机制诱导炎症状态,包括增加的瘦素表达,受损的肠粘膜和/或肠道微生物群破坏。涉及与肥胖有关的OA炎症的主要信号通路是蛋白酪氨酸磷酸酶1B(PTP1B)和TLR4或DAP12。此外,我们还强调了LPS植物提取物的污染作为研究HM对关节细胞的影响时考虑的重要因素。通过总结最近的出版物,本综述旨在突出新建立的肥胖方面,而不是机械之外的OA。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号