Protective effect of zinc supplementation on tricalcium phosphate particles-induced inflammatory osteolysis in mice,Microscopy Research and Technique

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Protective effect of zinc supplementation on tricalcium phosphate particles-induced inflammatory osteolysis in mice
Microscopy Research and Technique ( IF 2.0 ) Pub Date : 2022-07-25 , DOI: 10.1002/jemt.24213
Pei Yang ₁ , Tao Zhang ₁ , Ruirong Zhu ₁ , Yuchen Shen ₁ , Yuefang Pan ₁ , Yun Zhang ₁

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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)-α, interleukin (IL)-1β, 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 2α (eIF2α), phospho-eIF2α (p-eIF2α), activating transcription factor 4 (ATF4), inositol-requiring enzyme 1α (IRE1-α) and transcription factor X-box binding protein spliced (XBP1s), leading to decreasing the ratios of p-PERK/PERK and p-eIF2α/eIF2α. 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.

中文翻译：

补锌对磷酸三钙颗粒诱导小鼠炎症性骨溶解的保护作用

锌 (Zn) 是人体必需的微量元素，可刺激骨形成并抑制破骨细胞的骨吸收，从而控制骨骼的生长和维持。然而，补锌对磷酸三钙 (TCP) 磨损颗粒诱导的骨溶解的影响仍然未知。在这里，我们将 Zn 掺杂到 TCP 颗粒 (ZnTCP) 中，并探索 Zn 对 TCP 颗粒诱导的体内骨溶解的保护作用。TCP颗粒和ZnTCP颗粒包埋在小鼠颅盖骨中缝周围的骨膜下。2周后采集血液、骨膜组织和颅骨，测定血清锌和骨钙素、促炎细胞因子、骨生化标志物、破骨细胞生成和骨吸收面积，并解释其作用机制。数据显示，锌显着防止 TCP 颗粒诱导的破骨细胞生成和骨丢失，并增加骨转换。锌补充剂显着抑制了促炎细胞因子的释放，包括肿瘤坏死因子 (TNF)-α、白细胞介素 (IL)-1β 和 IL-6。免疫印迹表明 Zn 可减轻 ER 应激相关蛋白的表达水平，例如葡萄糖调节蛋白 78 (GRP78)、PKR 样 ER 激酶 (PERK)、磷酸化 PERK (p-PERK)、真核起始因子 2α (eIF2α)、磷酸-eIF2α (p-eIF2α)、激活转录因子 4 (ATF4)、肌醇需要酶 1α (IRE1-α) 和转录因子 X-box 结合蛋白剪接 (XBP1s)，导致 p-PERK/ 的比率降低PERK 和 p-eIF2α/eIF2α。综合起来，

更新日期：2022-07-25

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