A Study on the Mechanism of Amygdalin in Reducing the Occurrence of Osteoarthritis by Inhibiting the Differentiation of Th17 Cells and the Release of TGF-beta

作者：Duan, Liqun^*; Zhang, Wenzhi; Zhang, Feng; Cai, Haiping

来源：Journal of Biomaterials and Tissue Engineering, 2018, 8(9): 1301-1307.

DOI：10.1166/jbt.2018.1879

• Amygdalin
• Osteoarthritis
• Subchondral Cartilage
• TGF-beta Pathway
• Angiogenesis

Background: The present research aims to explore the pathogenesis of osteoarthritis through studying the role of Amygdalin in the transforming growth factor (TGF-beta) pathway, Th17 cell differentiation, and angiogenesis, thus providing preventive and clinical treatment for osteoarthritis with a new theoretical perspective. Material and Methods. The ACLT animal model was established, immunofluorescence assay was used to detect the change of Th17 cells in subchondral bone and the variation of RANKL amount. MSCs and phosphorylated smad2/3 were immuno-stained in vivo. The subchondral bone vascularity was verified by vascular imaging and immunofluorescence staining of CD31 and Endomucin. IMSCs were cultured in vitro, and Western Blot was applied to observe the effect of Amygdalin on TGF-beta pathway. Results: Amygdalin inhibited Th17 cells in the subchondral bone, reduced the bone resorption of subchondral bone abnormalities, decreased the release of excessive active TGF-beta, and inhibited the smad2/3 signaling pathway in TGF-beta of bone marrow mesenchymal stem cells. The inhibition of smad2/3 signaling pathway inhibited the formation of MSCs and also the abnormal blood vessel. Conclusion: Amygdalin can regulate bone remodeling of subchondral bone abnormalities and then inhibit the occurrence of osteoarthritis.

• 出版日期2018-9
• 单位中国科学技术大学