Potato protein hydrolysate inhibits RANKL-induced osteoclast development by inhibiting osteoclastogenic genes via the NF-κB/MAPKs signaling pathways

被引:1
作者
Chen, Yi-Ju [1 ,2 ]
He, Yen-Hua [3 ]
Lo, Yun-Hsin [3 ]
Yang, Hong-Siang [4 ]
Abomughaid, Mosleh Mohammad [5 ]
Kumar, K. J. Senthil [6 ,7 ]
Lin, Wan-Teng [4 ,8 ]
机构
[1] Taichung Vet Gen Hosp, Dept Surg, Taichung, Taiwan
[2] Tunghai Univ, Coll Agr & Hlth, Dept Anim Sci & Biotechnol, Taichung, Taiwan
[3] Tunghai Univ, Coll Agr & Hlth, Dept Food Sci, Taichung, Taiwan
[4] Tunghai Univ, Coll Agr & Hlth, Dept Hospitality Management, Taichung, Taiwan
[5] Univ Bisha, Coll Appl Med Sci, Dept Med Lab Sci, Bisha, Saudi Arabia
[6] Natl Chung Hsing Univ, Bachelor Program Biotechnol, Taichung, Taiwan
[7] Natl Chung Hsing Univ, Ctr Gen Educ, Taichung, Taiwan
[8] Utopia Holiday Hotel Corp, Res & Dev Div, Taichung, Taiwan
关键词
anti-osteoclast; HO-1; MAPK; NF-kappa B; osteoclast; peptides; potato protein hydrolysate; RANKL; DIFFERENTIATION; OSTEOPOROSIS; PEPTIDE;
D O I
10.1002/tox.24251
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
In recent times, there has been growing attention towards exploring the nutritional and functional aspects of potato protein, along with its diverse applications. In the present study, we examined the anti-osteoclast properties of potato protein hydrolysate (PP902) in vitro. Murine macrophages (RAW264.7) were differentiated into osteoclasts by receptor activator of nuclear factor-kappa B ligand (RANKL), and PP902 was examined for its inhibitory effect. Initially, treatment with PP902 was found to significantly prevent RANKL-induced morphological changes in macrophage cells, as determined by tartrate-resistant acid phosphatase (TRAP) staining analysis. This notion was further supported by F-actin analysis using a confocal microscope. Furthermore, PP902 treatment effectively and dose-dependently down-regulated the expression of RANKL-induced osteoclastogenic marker genes, including TRAP, CTR, RANK, NFATc1, OC-STAMP, and c-Fos. These inhibitory effects were associated with suppressing NF-kappa B transcriptional activation and subsequent reduced nuclear translocation. The decrease in NF-kappa B activity resulted from reduced activation of its upstream kinases, including I-kappa B alpha and IKK alpha. Moreover, PP902 significantly inhibited RANKL-induced p38MAPK and ERK1/2 activities. Nevertheless, PP902 treatment prevents RANKL-induced intracellular reactive oxygen species generation via increased HO-1 activity. The combined antioxidant and anti-inflammatory effects of PP902 resulted in significant suppression of osteoclastogenesis, suggesting its potential as an adjuvant therapy for osteoclast-related diseases.
引用
收藏
页码:3991 / 4003
页数:13
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