胶原蛋白肽通过增强成骨细胞分化和矿化来缓解雌激素缺乏引起的骨质疏松症。

Collagen peptides alleviate estrogen deficiency-induced osteoporosis by enhancing osteoblast differentiation and mineralization.

作者信息

Yang Qi, Mu Zhishen, Ma Xiaoyu, Yang Ximing, Fu Baifeng, Chang Zhihui, Cheng Shuzhen, Du Ming

机构信息

SKL of Marine Food Processing & Safety Control, School of Food Science and Technology, Dalian Polytechnic University, Dalian, China.

National Engineering Research Center of Seafood, Collaborative Innovation Center of Seafood Deep Processing, Dalian Polytechnic University, Dalian, China.

出版信息

J Sci Food Agric. 2025 Apr;105(6):3284-3295. doi: 10.1002/jsfa.14086. Epub 2024 Dec 20.

DOI:10.1002/jsfa.14086

PMID:39704042

Abstract

BACKGROUND

Osteoporosis is a systemic skeletal disorder characterized by decreased bone mass and impaired bone microarchitecture because of an imbalance between bone resorption and formation. Existing pharmacological treatments often have significant side effects and mainly focus on inhibiting bone resorption. Other than inhibiting osteoclast-mediated bone resorption, the present study also investigates the potential role of sheepskin collagen peptide (SSCP) in bone formation by promoting osteoblast proliferation, differentiation and mineralization.

RESULTS

SSCP improved bone mineral density in ovariectomized mice by improving bone volume, trabecular thickness and trabecular number. Histological analysis and tartrate-resistant acid phosphatase (TRAP) staining revealed denser trabeculae and decreased osteoclast activity, accompanied by a normalized receptor activator of nuclear factor kappa-B ligand/osteoprotegerin ratio and reduced serum TRAP levels. SSCP promotes the proliferation, differentiation and mineralization of MC3T3-E1 osteoblast cells by upregulating osteogenic markers such as bone morphogenetic protein (BMO)-2, runt-related transcription factor (RUNX)-2 and β-catenin. SSCP enhanced bone formation and suppressed bone resorption by activating the WNT/β-catenin and BMP/Smad signaling pathways.

CONCLUSION

SSCP offers a dual modulatory approach to bone health, addressing both bone formation and resorption. Its activation of key osteogenic pathways and improvement in bone structural integrity highlight its therapeutic potential for managing osteoporosis and enhancing skeletal health. By activating key osteogenic pathways and normalizing bone metabolism markers, SSCP presents a promising therapeutic candidate for osteoporosis and other bone-related conditions. Further clinical studies are needed to confirm these findings and explore its potential applications. © 2024 Society of Chemical Industry.

摘要

背景

骨质疏松症是一种全身性骨骼疾病，其特征是由于骨吸收和形成之间的不平衡导致骨量减少和骨微结构受损。现有的药物治疗通常有显著的副作用，且主要侧重于抑制骨吸收。除了抑制破骨细胞介导的骨吸收外，本研究还探讨了绵羊皮胶原蛋白肽（SSCP）通过促进成骨细胞增殖、分化和矿化在骨形成中的潜在作用。

结果

SSCP通过改善骨体积、小梁厚度和小梁数量提高了去卵巢小鼠的骨密度。组织学分析和抗酒石酸酸性磷酸酶（TRAP）染色显示小梁更密集，破骨细胞活性降低，同时核因子κB受体激活剂配体/骨保护素比值正常化，血清TRAP水平降低。SSCP通过上调骨形态发生蛋白（BMP）-2、 runt相关转录因子（RUNX）-2和β-连环蛋白等成骨标志物，促进MC3T3-E1成骨细胞的增殖、分化和矿化。SSCP通过激活WNT/β-连环蛋白和BMP/Smad信号通路增强骨形成并抑制骨吸收。