(−)-Epigallocatechin-3-gallate (EGCG) enhances healing of femoral bone defect

Previously, we found that (−)-epigallocatechin-3-gallate (EGCG) enhanced osteogenic differentiation of murine bone marrow mesenchymal stem cells by increasing the mRNA expression of osteogenesis-related genes, alkaline phosphatase activity and eventually mineralization. We further found EGCG supplem...

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Veröffentlicht in:Phytomedicine (Stuttgart) 2019-03, Vol.55, p.165-171
Hauptverfasser: Lin, Sung-Yen, Kang, Lin, Chen, Jian-Chih, Wang, Chau-Zen, Huang, Han Hsiang, Lee, Mon-Juan, Cheng, Tsung-Lin, Chang, Chi-Fen, Lin, Yi-Shan, Chen, Chung-Hwan
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Sprache:eng
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Zusammenfassung:Previously, we found that (−)-epigallocatechin-3-gallate (EGCG) enhanced osteogenic differentiation of murine bone marrow mesenchymal stem cells by increasing the mRNA expression of osteogenesis-related genes, alkaline phosphatase activity and eventually mineralization. We further found EGCG supplementation preserved bone mass and microarchitecture in female rats during estrogen deficiency in the proximal tibia and lumbar spine at least in part by increasing bone morphogenetic protein-2 (BMP2). BMP2 can enhance de novo bone formation. In this study, we evaluate the effect of local EGCG application in de novo bone formation in bone defect healing. Twenty-four rats aged 4 months were weight-matched and randomly allocated to 2 groups: defect control with vehicle treatment (control) and defect with 10 µM EGCG treatment (EGCG). Daily vehicle and EGCG were applied locally by percutaneous local injection 2 days after defect creation for 2 weeks. Four weeks after treatment, animals were sacrificed for micro-computed tomography (μ-CT) and biomechanical analysis. Local EGCG at femoral defect can enhance de novo bone formation by increasing bone volume and subsequently improve mechanical properties including max load, break point, stiffness, area under the max load curve, area under the break point curve and ultimate stress. Local EGCG may enhance bone defect healing via at least partly by the de novo bone formation of BMP-2. [Display omitted]
ISSN:0944-7113
1618-095X
DOI:10.1016/j.phymed.2018.07.012