Abstract：
BACKGROUND: The global increase in the aging population has led to a higher incidence of osteoporosis among the elderly.
OBJECTIVE: This study aimed to evaluate the protective properties of pinoresinol diglucoside (PDG), an active constituent of Eucommia ulmoides, against dexamethasone-induced osteoporosis and chondrodysplasia.
METHODS: A zebrafish model of osteoporosis was established by exposing larval zebrafish to dexamethasone. The impact of PDG on bone mineralization was assessed through alizarin red and calcein staining. Alkaline phosphatase activity was quantified to evaluate osteoblast function. The influence of PDG on chondrogenesis was estimated using alcian blue staining. Fluorescence imaging and motor behavior analysis were employed to assess the protective effect of PDG on the structure and function of dexamethasone-induced skeletal teratogenesis. qPCR determined the expression of osteogenesis and Wnt signaling-related genes. Molecular docking was used to assess the potential interactions between PDG and Wnt receptors.
RESULTS: PDG significantly increased bone mineralization and corrected spinal curvature and cartilage malformations in the zebrafish model. Furthermore, PDG enhanced swimming abilities compared to the model group. PDG mitigated dexamethasone-induced skeletal abnormalities in zebrafish by upregulating Wnt signaling, showing potential interaction with Wnt receptors FZD2 and FZD5.
CONCLUSIONS: PDG mitigates dexamethasone-induced osteoporosis and chondrodysplasia by promoting bone formation and activating Wnt signaling.
OBJECTIVE: This study aimed to evaluate the protective properties of pinoresinol diglucoside (PDG), an active constituent of Eucommia ulmoides, against dexamethasone-induced osteoporosis and chondrodysplasia.
METHODS: A zebrafish model of osteoporosis was established by exposing larval zebrafish to dexamethasone. The impact of PDG on bone mineralization was assessed through alizarin red and calcein staining. Alkaline phosphatase activity was quantified to evaluate osteoblast function. The influence of PDG on chondrogenesis was estimated using alcian blue staining. Fluorescence imaging and motor behavior analysis were employed to assess the protective effect of PDG on the structure and function of dexamethasone-induced skeletal teratogenesis. qPCR determined the expression of osteogenesis and Wnt signaling-related genes. Molecular docking was used to assess the potential interactions between PDG and Wnt receptors.
RESULTS: PDG significantly increased bone mineralization and corrected spinal curvature and cartilage malformations in the zebrafish model. Furthermore, PDG enhanced swimming abilities compared to the model group. PDG mitigated dexamethasone-induced skeletal abnormalities in zebrafish by upregulating Wnt signaling, showing potential interaction with Wnt receptors FZD2 and FZD5.
CONCLUSIONS: PDG mitigates dexamethasone-induced osteoporosis and chondrodysplasia by promoting bone formation and activating Wnt signaling.
摘要：
背景：全球老龄化人口的增加导致老年人骨质疏松症的发病率更高。
目的：本研究旨在评估松脂醇二葡糖苷（PDG）的保护特性，杜仲的活性成分，对抗地塞米松诱导的骨质疏松症和软骨发育不良。
方法：通过将斑马鱼幼体暴露于地塞米松，建立斑马鱼骨质疏松模型。通过茜素红和钙黄绿素染色评估PDG对骨矿化的影响。定量碱性磷酸酶活性以评估成骨细胞功能。使用阿尔辛蓝染色估计PDG对软骨形成的影响。荧光成像和运动行为分析用于评估PDG对地塞米松诱导的骨骼畸形发生的结构和功能的保护作用。qPCR检测成骨和Wnt信号相关基因的表达。分子对接用于评估PDG和Wnt受体之间的潜在相互作用。
结果：PDG在斑马鱼模型中显着增加了骨矿化，矫正了脊柱弯曲和软骨畸形。此外，与模型组相比，PDG增强了游泳能力。PDG通过上调Wnt信号减轻地塞米松诱导的斑马鱼骨骼异常，显示与Wnt受体FZD2和FZD5的潜在相互作用。
结论：PDG通过促进骨形成和激活Wnt信号，减轻地塞米松诱导的骨质疏松和软骨发育不良。
目的：本研究旨在评估松脂醇二葡糖苷（PDG）的保护特性，杜仲的活性成分，对抗地塞米松诱导的骨质疏松症和软骨发育不良。
方法：通过将斑马鱼幼体暴露于地塞米松，建立斑马鱼骨质疏松模型。通过茜素红和钙黄绿素染色评估PDG对骨矿化的影响。定量碱性磷酸酶活性以评估成骨细胞功能。使用阿尔辛蓝染色估计PDG对软骨形成的影响。荧光成像和运动行为分析用于评估PDG对地塞米松诱导的骨骼畸形发生的结构和功能的保护作用。qPCR检测成骨和Wnt信号相关基因的表达。分子对接用于评估PDG和Wnt受体之间的潜在相互作用。
结果：PDG在斑马鱼模型中显着增加了骨矿化，矫正了脊柱弯曲和软骨畸形。此外，与模型组相比，PDG增强了游泳能力。PDG通过上调Wnt信号减轻地塞米松诱导的斑马鱼骨骼异常，显示与Wnt受体FZD2和FZD5的潜在相互作用。
结论：PDG通过促进骨形成和激活Wnt信号，减轻地塞米松诱导的骨质疏松和软骨发育不良。
