Nodakenin Ameliorates Ovariectomy-Induced Bone Loss by Regulating Gut Microbiota

文献类型： 外文期刊

第一作者： Liu, Chunxiao

作者： Liu, Chunxiao;Wang, Zijiao;Li, Yueyao;Zhang, Yuanyuan;Li, Guangyu;Liu, Chunxiao;Chen, Jingyue

作者机构：

关键词： osteoporosis; nodakenin; gut microbiota; intestinal barrier; metabolomics

期刊名称：MOLECULES （ 影响因子：4.6； 五年影响因子：4.9 ）

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年卷期： 2024 年 29 卷 6 期

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收录情况： SCI

摘要： Disordered gut microbiota (GM) structure and function may contribute to osteoporosis (OP). Nodakenin has been shown to ameliorate osteoporosis; however, its anti-osteoporotic mechanism is unknown. This study aimed to further reveal the mechanism of the anti-osteoporotic action of nodakenin from the perspective of the microbiome and metabolome. An osteoporosis model was induced in mice through ovariectomy (OVX), with bone mass and microstructure assessed using mu CT. Subsequently, ELISA and histologic examination were used to detect biochemical indicators of bone conversion and intestinal morphology. Using metabolomics and 16S rRNA sequencing, it was possible to determine the composition and abundance of the gut microbiota in feces. The results revealed that nodakenin treatment improved the bone microstructure and serum levels of bone turnover markers, and increased the intestinal mucosal integrity. 16S rRNA sequencing analysis revealed that nodakenin treatment decreased the relative abundance of Firmicutes and Patescibacteria, as well as the F/B ratio, and elevated the relative abundance of Bacteroidetes in OVX mice. In addition, nodakenin enhanced the relative abundance of Muribaculaceae and Allobaculum, among others, at the genus level. Moreover, metabolomics analysis revealed that nodakenin treatment significantly altered the changes in 113 metabolites, including calcitriol. A correlation analysis revealed substantial associations between various gut microbiota taxa and both the osteoporosis phenotype and metabolites. In summary, nodakenin treatment alleviated OVX-induced osteoporosis by modulating the gut microbiota and intestinal barrier.

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