Academic Journal

Toddalolactone protects against osteoarthritis by ameliorating chondrocyte inflammation and suppressing osteoclastogenesis

التفاصيل البيبلوغرافية
العنوان: Toddalolactone protects against osteoarthritis by ameliorating chondrocyte inflammation and suppressing osteoclastogenesis
المؤلفون: Yiming Xu, Song Xue, Tian Zhang, Xinmeng Jin, Cong Wang, Haiming Lu, Yiming Zhong, Hongjie Chen, Libo Zhu, Jinzhong Ma, Weilin Sang
المصدر: Chinese Medicine, Vol 17, Iss 1, Pp 1-16 (2022)
بيانات النشر: BMC, 2022.
سنة النشر: 2022
المجموعة: LCC:Other systems of medicine
مصطلحات موضوعية: Toddalolactone, Cartilage, Inflammation, Osteoclastogenesis, Osteoarthritis, Other systems of medicine, RZ201-999
الوصف: Abstract Background Osteoarthritis (OA) is widely recognized as the most common chronic joint disease accompanied by progressive cartilage and subchondral bone damage. Toddalolactone (TOD), a natural compound extracted from Toddalia asiatica (L.) Lam., has been widely used in the treatment of stroke, rheumatoid arthritis, and oedema. Nevertheless, what TOD acts as in the pathogenesis and progression of OA hasn’t been reported. In this investigation, we have aimed to determine how TOD affects OA in vitro and in vivo. Methods LPS (10 µg/ml) and IL-1β (10 ng/ml) were employed to induce chondrocyte inflammation or RANKL to induce osteoclast differentiation in bone marrow derived macrophages (BMMs). The effects of TOD on chondrocyte inflammation and osteoclast differentiation were evaluated. Anterior cruciate ligament transection (ACLT) was performed to develop an OA animal model and study the effects of TOD. Results We found that TOD inhibited the expression of inflammatory and catabolic mediators (IL-6, IL-8, TNF-α, MMP2, MMP9, and MMP13) in inflammatory chondrocytes in vitro. Furthermore, TOD was proven to inhibit RANKL-induced-osteoclastogenesis and inhibit the expression of osteoclast marker genes. Our data also confirmed that TOD suppressed the destruction of articular cartilage and osteoclastogenesis via inhibiting the activation of NF-κB and MAPK signalling pathways. In the ACLT mouse model, we found that TOD attenuated cartilage erosion and inhibited bone resorption. Conclusions These results showed that TOD can be adopted as a potential therapeutic agent for OA.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1749-8546
Relation: https://doaj.org/toc/1749-8546
DOI: 10.1186/s13020-022-00576-w
URL الوصول: https://doaj.org/article/ea4d943ee8fb42b8813f28abde0329fc
رقم الانضمام: edsdoj.4d943ee8fb42b8813f28abde0329fc
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:17498546
DOI:10.1186/s13020-022-00576-w