ArticleImmunity, inflammation and disease2026
Didymin may Enhance Tendon-Bone Healing Partly by Promoting PPAR-Mediated Fatty Acid Oxidation and Macrophage M2 Polarization.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveAchieving 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.
methodsA 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.
resultsTreatment 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.
conclusionThis 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.
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