ArticleApplied biochemistry and biotechnology2026
Total Flavonoids of Rhizoma Drynariae Ameliorate Tendon-Bone Healing Following Anterior Cruciate Ligament Reconstruction in Rats by Activating the FSP1/CoQ
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
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3 authors.
Funding
Abstract
Objective Poor tendon-bone healing after anterior cruciate ligament reconstruction (ACLR) is often accompanied by impaired osteogenesis and apoptosis, while iron overload and mitochondrial dysfunction may exacerbate this process through ferroptosis. Although total flavonoids of Rhizoma Drynariae (TFRD) are known to have osteogenesis-promoting effects, whether they improve tendon-bone healing by regulating ferroptosis remains unclear. Methods The impact of TFRD on bone formation, ferroptosis, and mitochondrial function was evaluated using an ACLR rat model and a Dexamethasone (Dex)-induced osteoblast injury model. Hematoxylin and Eosin (H&E), Masson, and Alizarin Red staining were used to examine pathological changes at the tendon‑bone interface and osteogenic mineralization. Western blot and immunohistochemistry were performed to assess the protein expression levels of runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), and collagen I (Col I). Quantification of iron levels, malondialdehyde, glutathione, superoxide dismutase, adenosine triphosphate, and CoQ10 were quantified with specific assay kits. Mitochondrial membrane potential and respiratory function were analyzed by JC-1 staining and oxygen consumption rate (OCR) measurements, respectively. The underlying mechanisms were further investigated using a ferroptosis-suppressing protein 1 (FSP1) inhibitor iFSP1 and the ferroptosis inhibitor Fer-1. Results TFRD markedly increased bone mineral density and upregulated the expression of RUNX2, OCN, and Col I in ACLR rats, while also improving fibrin arrangement and calcification. Moreover, TFRD reduced iron accumulation, lipid peroxidation, and mitochondrial damage, and activated the FSP1/CoQ
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