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大车前苷抑制核因子κB和丝裂原活化蛋白激酶的激活,并改善骨关节炎的发展。

Plantamajoside suppresses the activation of NF-κB and MAPK and ameliorates the development of osteoarthritis.

作者信息

Lin Shida, Lu Jiajie, Chen Qiaoxue, Jiang Hongyi, Lou Chao, Lin Chihao, Wang Weidan, Lin Jian, Pan Xiaoyun, Xue Xinghe

机构信息

Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China; Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, Zhejiang Province, China; The Second School of Medicine, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.

Department of Emergency Medicine, The First Affiliate Hospital of Guang Zhou Medical University, Guangzhou, Guangdong 510120, China.

出版信息

Int Immunopharmacol. 2023 Feb;115:109582. doi: 10.1016/j.intimp.2022.109582. Epub 2022 Dec 28.

DOI:10.1016/j.intimp.2022.109582
PMID:36584575
Abstract

Osteoarthritis (OA) is a common degenerative bone and joint disorder characterized by progressive cartilage degeneration and secondary synovial inflammation. It is a common chronic joint disorder that affects people of all ages (especially the old). Plantamajoside is a phenylpropanoside derived from plantain. It has a variety of biological properties, including antioxidant, anti-malignant cell proliferation, and anti-inflammatory properties. In this study, the latent mechanism of plantamajoside was explored by slowing the in-vivo and in-vitro progression of osteoarthritis. The results revealed that plantamajoside pre-conditioning inhibited IL-1β induced pro-inflammatory factors like COX-2, iNOS, IL-6, and TNF-α. Moreover, plantamajoside also reversed the IL-1 β mediated type II collagen and aggrecan degradation within the extracellular matrix (ECM). The protective effects of plantamajoside have been attributed to the inhibition of both MAPK and NF-κB pathways. Furthermore, our in-vivo research found that plantamajoside could slow the progression of OA in mice. Finally, all findings point to plantamajoside as a potential anti-OA therapeutic candidate.

摘要

骨关节炎(OA)是一种常见的退行性骨和关节疾病,其特征为进行性软骨退变和继发性滑膜炎。它是一种常见的慢性关节疾病,影响所有年龄段的人(尤其是老年人)。大车前苷是一种从车前草中提取的苯丙素苷。它具有多种生物学特性,包括抗氧化、抗恶性细胞增殖和抗炎特性。在本研究中,通过减缓骨关节炎的体内和体外进展来探索大车前苷的潜在作用机制。结果显示,大车前苷预处理可抑制白细胞介素-1β(IL-1β)诱导的促炎因子,如环氧合酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)。此外,大车前苷还可逆转IL-1β介导的细胞外基质(ECM)中II型胶原蛋白和聚集蛋白聚糖的降解。大车前苷的保护作用归因于对丝裂原活化蛋白激酶(MAPK)和核因子κB(NF-κB)途径的抑制。此外,我们的体内研究发现,大车前苷可减缓小鼠骨关节炎的进展。最后,所有研究结果均表明大车前苷是一种潜在的抗骨关节炎治疗候选药物。

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