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大豆肽通过 Smad 和 MAPK 信号通路改善 TGF-β1 介导的成骨细胞分化。

Soy Peptide Ameliorate TGF-β1-Mediated Osteoblast Differentiation through Smad and MAPK Signaling Pathways.

机构信息

College of Life Science, Yantai University, Yantai, Shandong 264000, China.

Beijing Key Laboratory of Functional Food from Plant Resources, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.

出版信息

J Agric Food Chem. 2024 Oct 23;72(42):23246-23257. doi: 10.1021/acs.jafc.4c04882. Epub 2024 Oct 11.

Abstract

The aim of this study was to determine the osteogenic activity and mechanism of soybean peptide VVELLKAFEEKF (SOP) and the potential relationship between SOP and transforming growth factor-β1 (TGF-β1). The results show that SOP promotes MC3T3-E1 cell proliferation by altering cell progression. SOP induced cell differentiation and mineralization in a dose-dependent manner at 0.7-7 μM. Moreover, SOP stimulates osteoblast differentiation, which may be achieved through the activation of p38-MAPK and Smad2/3 signaling pathways. Furthermore, treatment with a TβRI inhibitor (SB525334) inhibited the phosphorylation levels of p38 and Smad2/3, which indicates the involvement of TβRI in the process of osteoblast differentiation caused by SOP. Besides, in non-FBS-cultured MC3T3-E1 cells, SOP and TGF-β1 promoted the phosphorylation of Smad2/3 and alkaline phosphatase (ALP) activity, but the effect was lost when SOP was incubated separately, indicating that SOP stimulated osteoblast differentiation by promoting TGF-β1 activity. , SOP significantly restores bone mineral density loss and behavioral deficits in a model of glucocorticoid-induced osteoporosis (GIOP) in zebrafish. These results suggest that SOP may have the function of promoting bone remodeling and may be used as a potential active factor for functional food development to prevent osteoporosis.

摘要

本研究旨在确定大豆肽 VVELLKAFEEKF(SOP)的成骨活性和机制,以及 SOP 与转化生长因子-β1(TGF-β1)之间的潜在关系。结果表明,SOP 通过改变细胞进程促进 MC3T3-E1 细胞增殖。SOP 在 0.7-7 μM 范围内以剂量依赖的方式诱导细胞分化和矿化。此外,SOP 刺激成骨细胞分化,这可能是通过激活 p38-MAPK 和 Smad2/3 信号通路实现的。此外,用 TβRI 抑制剂(SB525334)处理可抑制 p38 和 Smad2/3 的磷酸化水平,表明 TβRI 参与了 SOP 诱导的成骨细胞分化过程。此外,在不含 FBS 的 MC3T3-E1 细胞中,SOP 和 TGF-β1 促进了 Smad2/3 的磷酸化和碱性磷酸酶(ALP)活性,但当 SOP 单独孵育时,该作用消失,表明 SOP 通过促进 TGF-β1 活性刺激成骨细胞分化。此外,SOP 可显著恢复斑马鱼糖皮质激素诱导的骨质疏松症(GIOP)模型中的骨密度损失和行为缺陷。这些结果表明,SOP 可能具有促进骨重塑的功能,可作为开发预防骨质疏松症的功能性食品的潜在活性因子。

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