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Dendrobine attenuates osteoclast differentiation through modulating ROS/NFATc1/ MMP9 pathway and prevents inflammatory bone destruction.冬凌草甲素通过调控 ROS/NFATc1/MMP9 通路抑制破骨细胞分化，进而防治炎症性骨破坏。
Phytomedicine. 2022 Feb;96:153838. doi: 10.1016/j.phymed.2021.153838. Epub 2021 Nov 6.
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MT2通过清除活性氧抑制破骨细胞生成。

MT2 INHIBITS OSTEOCLASTOGENESIS BY SCAVENGING ROS.

作者信息

Wei S, Liu K, Wu H, Hu J, He J, Li G, Liu B, Yang W

机构信息

Liuzhou Workers' Hospital, Liuzhou, Guangxi.

Fuzhou City Second Hospital, Fuzhou, China.

出版信息

Acta Endocrinol (Buchar). 2023 Oct-Dec;19(4):447-455. doi: 10.4183/aeb.2023.447. Epub 2024 Jun 24.

DOI:10.4183/aeb.2023.447
PMID:38933247
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11197834/
Abstract

CONTEXT AND OBJECTIVE

Reactive oxygen species (ROS) produced under oxidative stress is important for osteoclastogenesis. As a major member of the metallothionein (MT) family, metallothionein2 (MT2) can scavenge ROS in osteoblasts. However, the role of MT2 in osteoclastogenesis and ROS production in osteoclast precursors (OCPs) is unknown.

MATERIAL AND METHODS

In this study, we first investigated MT2 expression level in osteoporotic model mice. Next, we explored the roles of MT2 in osteoclastic differentiation and ROS production in OCPs. Ultimately, via rescue assays based on hydrogen peroxide (HO), the significance of ROS in MT-2-regulated osteoclastic differentiation was further elucidated.

RESULTS

Compared with sham operated (Sham) mice, ovariectomized (OVX) mice displayed bone marrow primary OCPs (Ly6C+CD11b-) having higher ROS levels and lower MT2 expression. MT2 overexpression inhibited the formation of mature osteoclasts, while MT2 knockdown was contrary. Moreover, MT2 overexpression inhibited ROS production in OCPs, while MT2 knockdown exhibited the opposite effects. Notably, the inhibitory effect of MT2 overexpression on osteoclastogenesis and ROS production was blocked by the addition of HO.

CONCLUSION

MT2 inhibits osteoclastogenesis through repressing ROS production in OCPs, which indicates that the strategy of upregulating MT2 in OCPs may be applied to the clinical treatment of osteoclastic bone loss.

摘要

背景与目的

氧化应激下产生的活性氧（ROS）对破骨细胞生成很重要。作为金属硫蛋白（MT）家族的主要成员，金属硫蛋白2（MT2）可清除成骨细胞中的ROS。然而，MT2在破骨细胞生成以及破骨细胞前体（OCPs）中ROS产生方面的作用尚不清楚。

材料与方法

在本研究中，我们首先调查了骨质疏松模型小鼠中MT2的表达水平。接下来，我们探究了MT2在OCPs破骨细胞分化和ROS产生中的作用。最终，通过基于过氧化氢（HO）的挽救实验，进一步阐明了ROS在MT-2调节的破骨细胞分化中的意义。

结果

与假手术（Sham）小鼠相比，去卵巢（OVX）小鼠的骨髓原代OCPs（Ly6C+CD11b-）具有更高的ROS水平和更低的MT2表达。MT2过表达抑制成熟破骨细胞的形成，而MT2敲低则相反。此外，MT2过表达抑制OCPs中ROS的产生，而MT2敲低则表现出相反的效果。值得注意的是，添加HO可阻断MT2过表达对破骨细胞生成和ROS产生的抑制作用。

结论

MT2通过抑制OCPs中ROS的产生来抑制破骨细胞生成，这表明上调OCPs中MT2的策略可能应用于破骨性骨质流失的临床治疗。