Immunity, inflammation and disease · 2026
Didymin may Enhance Tendon-Bone Healing Partly by Promoting PPAR-Mediated Fatty Acid Oxidation and Macrophage M2 Polarization.
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Ma Xiaojun, Shen Jia, Ma Jun, Li Hangyu, Li Yang, Wan Jun
Аннотация
OBJECTIVE: Achieving rapid and high-quality regeneration after injury at the tendon-bone interface remains an urgent challenge in the fields of orthopedics, sports medicine, and tissue regeneration. Didymin (DID) possesses a range of pharmacological activities, including anti-inflammatory, antioxidant, and antimicrobial properties; however, there is a research gap regarding the role of DID in tendon-bone healing. Therefore, this study intends to further investigate the role of DID in tendon-bone healing.
METHODS: A tendon-bone healing mouse model of Achilles tendon-Achilles bone was constructed, and the mice were treated with different doses of DID. The therapeutic effect of DID on tendon-bone healing and its effect on macrophage polarization were investigated by evaluating various parameters such as tendon-bone healing, fibrocartilage formation at the tendon-bone interface, and macrophage polarization. In addition, in vitro experiments were used to verify whether the PPAR-mediated fatty acid oxidation (FAO) pathway was involved in the induction of macrophage polarization by DID.
RESULTS: Treatment with DID was found to promote fibrocartilage formation in tendon-bone junction tissues, ameliorate pathological injuries, induced macrophage polarization towards the M2 type, and downregulate the levels of IL-1β and IL-6, while upregulating the levels of Arg1, IL-10, CoA, PPAR, and RXRA. However, the addition of a PPAR-γ antagonist (GW9662) or an FAO inhibitor (Etomoxir) significantly attenuated the effects of DID on macrophage polarization.
CONCLUSION: This study demonstrates that DID may enhance histological and molecular features of tendon-bone healing partly through PPAR-mediated fatty acid oxidation and macrophage M2 polarization, thereby facilitating tendon bone healing, with potential application value.
METHODS: A tendon-bone healing mouse model of Achilles tendon-Achilles bone was constructed, and the mice were treated with different doses of DID. The therapeutic effect of DID on tendon-bone healing and its effect on macrophage polarization were investigated by evaluating various parameters such as tendon-bone healing, fibrocartilage formation at the tendon-bone interface, and macrophage polarization. In addition, in vitro experiments were used to verify whether the PPAR-mediated fatty acid oxidation (FAO) pathway was involved in the induction of macrophage polarization by DID.
RESULTS: Treatment with DID was found to promote fibrocartilage formation in tendon-bone junction tissues, ameliorate pathological injuries, induced macrophage polarization towards the M2 type, and downregulate the levels of IL-1β and IL-6, while upregulating the levels of Arg1, IL-10, CoA, PPAR, and RXRA. However, the addition of a PPAR-γ antagonist (GW9662) or an FAO inhibitor (Etomoxir) significantly attenuated the effects of DID on macrophage polarization.
CONCLUSION: This study demonstrates that DID may enhance histological and molecular features of tendon-bone healing partly through PPAR-mediated fatty acid oxidation and macrophage M2 polarization, thereby facilitating tendon bone healing, with potential application value.