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Frugoside delays osteoarthritis progression via inhibiting miR-155-modulated synovial macrophage M1 polarization.
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- Author(s): Wang, Hao; Zhang, Haiyan; Fan, Kai; Zhang, Danyang; Hu, Aihau; Zeng, Xiangzhou; Liu, Yan li; Tan, Guanghong; Wang, Hua
- Source:
Rheumatology; Oct2021, Vol. 60 Issue 10, p4899-4909, 11p- Subject Terms:
DISEASE progression; PROTEINS; IN vitro studies; CYTOKINES; FLOW cytometry; CARTILAGE cells; MEDICINAL plants; SYNOVITIS; IN vivo studies; CELL culture; ANIMAL experimentation; INFLAMMATION; WESTERN immunoblotting; IMMUNOHISTOCHEMISTRY; GLYCOSIDES; MICRORNA; MACROPHAGES; PROTEOLYTIC enzymes; GENE expression; OSTEOARTHRITIS; MESSENGER RNA; INTRA-articular injections; FLUORESCENT antibody technique; TUMOR necrosis factors; POLYMERASE chain reaction; MICE - Source:
- Additional Information
- Abstract: Objectives Direct inhibition of M1 polarization of synovial macrophages may be a useful therapeutic treatment for OA and OA-associated synovitis. Frugoside (FGS) is a cardiac glycoside compound isolated and extracted from Calotropis gigantea. Cardiac glycosides possess interesting anti-inflammatory potential. However, the corresponding activity of FGS has not been reported. Therefore, our aim was to find direct evidence of the effects of FGS on synovial macrophage M1 polarization and OA control. Methods Collagenase was used to establish an experimental mouse OA model (CIOA) with considerable synovitis. Then, FGS was intra-articular administered. The mRNA and protein levels of iNOS were analysed by real-time PCR and Western blotting in vitro. Immunohistochemical and immunofluorescence staining were used to measure the expression of F4/80, iNOS, Col2α1 and MMP13 in vivo. The levels of pro-inflammatory cytokines in FGS-treated M1 macrophage culture supernatants were analysed by flow cytometry. Results FGS attenuates synovial inflammation and delays the development of OA in CIOA mice. Further results demonstrate that FGS inhibits macrophage M1 polarization in vitro and in vivo , which subsequently decreases the secretion of IL‐6 and TNF‐α, in turn delaying cartilage and extracellular matrix (ECM) degradation and chondrocyte hypertrophy. FGS inhibits macrophage M1 polarization by partially downregulating miR-155 levels. Conclusion This study demonstrates that intra-articular injection of FGS is a potential strategy for OA prevention and treatment, even at an early stage of disease progression. This is a novel function of FGS and has promising future clinical applications. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Rheumatology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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