Polydatin accelerates osteoporotic bone repair by inducing the osteogenesis-angiogenesis coupling of bone marrow mesenchymal stem cells via the PI3K/AKT/GSK-3β/β-catenin pathway.
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Abstract
Background: Polydatin (POL), a natural stilbenoid, has multiple pharmacological activities. However, its effect on osteoporotic bone defect has not yet been examined. This study was designed to explore the unknown role of POL on osteoporotic bone repair.
Methods: The effect of POL on osteogenesis and angiogenesis were investigated firstly. Then a series of angiogenesis-related assays were carried out to explore the relationship between osteogenesis and angiogenesis of POL, and the underlying mechanism was further explored. Whereafter, ovariectomy-induced osteoporosis rats with bone defect were treated with POL or placebo, the imageological and histological examinations were conducted to assess the effect of POL on osteoporotic bone repair.
Results: The moderate concentrations (1 μM and 10 μM) of POL enhanced osteogenesis of bone marrow mesenchymal stem cells (BMSCs) and elevated the expression of angiogenic-specific markers. Further research found that POL induced human umbilical vein endothelial cells migration and tube formation through the osteogenesis-angiogenesis coupling of BMSCs, and the POL-induced osteogenesis-angiogenesis coupling was reversed after co-cultured with LY294002, Mechanistically, this was conducted via activating PI3K/AKT/GSK-3β/β-catenin pathway. After that, using osteoporotic bone defect rat model, we observed that POL facilitated osteoporotic bone repair through enhancing osteogenesis and CD31hiEMCNhi type H-positive vessels formation via the PI3K/AKT/GSK-3β/β-catenin pathway.
Conclusion: The data above indicated that POL could accelerate osteoporotic bone repair by inducing the osteogenesis-angiogenesis coupling of BMSCs via the PI3K/AKT/GSK-3β/β-catenin pathway, which provided new insight and strategy for osteoporotic bone repair.
背景：多靛酚（POL）是一种天然类芪类化合物，具有多种药理活性。然而，它对骨质疏松性骨缺损的影响尚未得到研究。本研究旨在探索 POL 对骨质疏松性骨修复的未知作用：方法：首先研究 POL 对骨生成和血管生成的影响。方法：首先研究了 POL 对骨生成和血管生成的影响，然后进行了一系列血管生成相关试验，以探讨 POL 的骨生成和血管生成之间的关系，并进一步探索其潜在机制。之后，用 POL 或安慰剂治疗卵巢切除诱导的骨质疏松症大鼠的骨缺损，并进行影像学和组织学检查，以评估 POL 对骨质疏松症骨修复的影响：结果：中等浓度（1 μM和10 μM）的POL增强了骨髓间充质干细胞（BMSCs）的成骨能力，并提高了血管生成特异性标志物的表达。进一步研究发现，POL通过BMSCs的成骨-血管生成耦合诱导人脐静脉内皮细胞迁移和管形成，而与LY294002共培养后，POL诱导的成骨-血管生成耦合被逆转，其机制是通过激活PI3K/AKT/GSK-3β/β-catenin通路进行的。随后，我们利用骨质疏松性骨缺损大鼠模型观察到，POL通过PI3K/AKT/GSK-3β/β-catenin途径促进骨生成和CD31hiEMCNhi H型阳性血管形成，从而促进骨质疏松性骨修复：上述数据表明，POL可通过PI3K/AKT/GSK-3β/β-catenin通路诱导BMSCs的成骨-血管生成耦合，从而加速骨质疏松症骨修复，为骨质疏松症骨修复提供了新的思路和策略。
期刊介绍：
The International Journal of Surgery (IJS) has a broad scope, encompassing all surgical specialties. Its primary objective is to facilitate the exchange of crucial ideas and lines of thought between and across these specialties.By doing so, the journal aims to counter the growing trend of increasing sub-specialization, which can result in "tunnel-vision" and the isolation of significant surgical advancements within specific specialties.
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