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Protective effect of zinc supplementation on tricalcium phosphate particles-induced inflammatory osteolysis in mice  ( SCI-EXPANDED收录)   被引量:2

文献类型:期刊文献

英文题名:Protective effect of zinc supplementation on tricalcium phosphate particles-induced inflammatory osteolysis in mice

作者:Yang, Pei[1];Zhang, Yun[1];Zhang, Tao[1];Zhu, Ruirong[1];Shen, Yuchen[1];Pan, Yuefang[1]

机构:[1]Shaoxing Univ, Coll Med, Huancheng West Rd 508, Shaoxing 312000, Peoples R China

年份:0

外文期刊名:MICROSCOPY RESEARCH AND TECHNIQUE

收录:SCI-EXPANDED(收录号:WOS:000830465100001)、、Scopus(收录号:2-s2.0-85134558941)、WOS

基金:This work was supported by Natural Science Foundation of Zhejiang Province (LY21H060001) and National Natural Science Foundation of China (30900301).

语种:英文

外文关键词:ER stress; osteoclastogenesis; osteolysis; TCP particles; ZnTCP particles

外文摘要:Zinc (Zn), an essential trace element, can stimulate bone formation and inhibit osteoclastic bone resorption, which controls the growth and maintenance of bone. However, the effect of Zn supplementation on tricalcium phosphate (TCP) wear particles-induced osteolysis remains unknown. Here, we doped Zn into TCP particles (ZnTCP), and explore the protective effects of Zn on TCP particles-induced osteolysis in vivo. TCP particles and ZnTCP particles were embedded under the periosteum around the middle suture of the mouse calvaria. After 2 weeks, blood, the periosteal tissue, and the calvaria were collected to determine serum levels of Zn and osteocalcin, pro-inflammatory cytokines, bone biochemical markers, osteoclastogenesis and bone resorption area, and to explain its mechanism. Data revealed that Zn significantly prevented TCP particles-induced osteoclastogenesis and bone loss, and increased bone turnover. The Zn supplement remarkably suppressed the release of pro-inflammatory cytokines including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6. Immunoblotting demonstrated that Zn alleviated expression levels of ER stress-related proteins such as glucose-regulated protein 78 (GRP78), PKR-like ER kinase (PERK), phospho-PERK (p-PERK), eukaryotic initiation factor 2 alpha (eIF2 alpha), phospho-eIF2 alpha (p-eIF2 alpha), activating transcription factor 4 (ATF4), inositol-requiring enzyme 1 alpha (IRE1-alpha) and transcription factor X-box binding protein spliced (XBP1s), leading to decreasing the ratios of p-PERK/PERK and p-eIF2 alpha/eIF2 alpha. Taken together, Zn supplementation strongly prevents TCP particles-induced periprosthetic osteolysis via inhibition of the ER stress pathway, and it may be a novel therapeutic approach for the treatment of aseptic prosthesis loosening.

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