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Abstract：
This study aimed to explore naringin\'s potential to promote the osteogenic differentiation of MC3T3-E1 under oxidative stress. It delved into Nar\'s connection with the Wnt/β-catenin and PI3K/Akt signaling pathways. Initially, 2911 OP-related genes were analyzed, revealing close ties with the PI3K/Akt and Wnt pathways alongside oxidative stress. Nar\'s potential targets-ESR1, HSP90AA1, and ESR2-were identified through various databases and molecular docking studies confirmed Nar\'s affinity with ESR1 and HSP90AA1. Experiments established optimal concentrations for Nar and H2O2. H2O2 at 0.3 mmol/L damaged MC3T3-E1 cells, alleviated by 0.1 µmol/L Nar. Successful establishment of oxidative stress models was confirmed by DCFH-DA probe and NO detection. Nar exhibited the ability to enhance osteogenic differentiation, counteracting oxidative damage. It notably increased osteoblast-related protein expression in MC3T3-E1 cells under oxidative stress. The study found Nar\'s positive influence on GSK-3β phosphorylation, β-catenin accumulation, and pathway-related protein expression, all critical in promoting osteogenic differentiation. The research concluded that Nar effectively promotes osteogenic differentiation in MC3T3-E1 cells under oxidative stress. It achieved this by activating the Wnt/β-catenin and PI3K/Akt pathways, facilitating GSK-3β phosphorylation, and enhancing β-catenin accumulation, pivotal in osteogenesis.
摘要：
本研究旨在探讨柚皮苷在氧化应激下促进MC3T3-E1成骨分化的潜能。它探讨了Nar与Wnt/β-catenin和PI3K/Akt信号通路的联系。最初，分析了2911个OP相关基因，揭示与PI3K/Akt和Wnt途径以及氧化应激密切相关。通过各种数据库和分子对接研究确定了Nar的潜在靶标ESR1，HSP90AA1和ESR2，证实了Nar与ESR1和HSP90AA1的亲和力。实验确定了Nar和H2O2的最佳浓度。0.3mmol/LH2O2损伤MC3T3-E1细胞，由0.1μmol/LNar缓解。通过DCFH-DA探针和NO检测证实了氧化应激模型的成功建立。Nar表现出增强成骨分化的能力，抵消氧化损伤。在氧化应激下，它显着增加了MC3T3-E1细胞中成骨细胞相关蛋白的表达。研究发现Nar对GSK-3β磷酸化有积极影响，β-连环蛋白积累，和通路相关蛋白表达，都是促进成骨分化的关键。研究结论：Nar能有效促进MC3T3-E1细胞在氧化应激下的成骨分化。它通过激活Wnt/β-catenin和PI3K/Akt途径实现了这一点，促进GSK-3β磷酸化，并增强β-连环蛋白的积累，在成骨过程中至关重要。
