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4-己基间苯二酚通过抑制NF-κB信号通路抑制破骨细胞生成,并逆转去卵巢小鼠的骨质流失。

4-Hexylresorcinol inhibits osteoclastogenesis by suppressing the NF-κB signaling pathway and reverses bone loss in ovariectomized mice.

作者信息

Yi Wenkai, Liu Tao, Gao Xinfeng, Xie Yonghua, Liu Ming

机构信息

Department of Spine Surgery, Pu Ai Hospital of Wuhan City, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430000, P.R. China.

出版信息

Exp Ther Med. 2021 Apr;21(4):354. doi: 10.3892/etm.2021.9785. Epub 2021 Feb 11.

DOI:10.3892/etm.2021.9785
PMID:33732327
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7903454/
Abstract

4-Hexylresorcinol (4HR) is a small organic compound that is widely used as an antiseptic and antioxidant. In the present study, its role in osteoclastogenesis was investigated. Bone marrow-derived macrophages from mice were used to examine the role of 4HR in osteogenesis. An ovariectomy (OVX) mouse model was constructed to examine the effect of 4HR , followed by hematoxylin and eosin and tartrate resistant acid phosphatase staining. In the present study, 4HR effectively suppressed receptor activator of NF-κB ligand-induced osteoclastogenesis in a dose-dependent manner. 4HR was also found to significantly suppress the expression of osteoclast (OC)-specific markers, including tartrate-resistant acid phosphatase, cathepsin K, nuclear factor of activated T-cell cytoplasmic 1 and c-Fos in the presence of RANKL in BMMs. Furthermore, 4HR inhibited osteoclastogenesis by inhibiting the activation of the NF-κB signaling pathway in BMMs. Consistent with the results, 4HR effectively ameliorated OVX-induced bone loss and markedly reduced OC number in the proximal tibia . In conclusion, the present results suggested that 4HR inhibited osteoclastogenesis and rescued bone loss , suggesting that 4HR may serve as a novel therapeutic agent for osteoporosis treatment.

摘要

4-己基间苯二酚(4HR)是一种小型有机化合物,被广泛用作防腐剂和抗氧化剂。在本研究中,对其在破骨细胞生成中的作用进行了研究。使用来自小鼠的骨髓源性巨噬细胞来检测4HR在成骨中的作用。构建卵巢切除(OVX)小鼠模型以检测4HR的作用,随后进行苏木精和伊红染色以及抗酒石酸酸性磷酸酶染色。在本研究中,4HR以剂量依赖性方式有效抑制核因子κB受体活化因子配体诱导的破骨细胞生成。还发现4HR在存在RANKL的情况下,能显著抑制骨髓巨噬细胞(BMMs)中破骨细胞(OC)特异性标志物的表达,包括抗酒石酸酸性磷酸酶、组织蛋白酶K、活化T细胞核因子细胞质1和c-Fos。此外,4HR通过抑制BMMs中NF-κB信号通路的激活来抑制破骨细胞生成。与这些结果一致,4HR有效改善了OVX诱导的骨质流失,并显著减少了胫骨近端的OC数量。总之,目前的结果表明4HR抑制破骨细胞生成并挽救骨质流失,这表明4HR可能作为一种新型治疗药物用于骨质疏松症的治疗。

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