促炎细胞因子
骨吸收
Wnt信号通路
肠道菌群
骨质疏松症
化学
骨矿物
信号转导
糖皮质激素
内分泌学
连环素
益生元
内科学
骨重建
生物
细胞生物学
炎症
生物化学
医学
作者
Jingjing Li,Mingyuan Yang,Chenyang Lu,Jiaojiao Han,Shasha Tang,Jun Zhou,Ye Li,Tinghong Ming,Zaijie Jim Wang,Xiurong Su
标识
DOI:10.1002/mnfr.201900861
摘要
Scope The effects and mechanism of tuna bone powder (TBP) on glucocorticoid‐induced osteoporosis (GIOP) alleviation in terms of signaling pathway coregulation and gut microbiota modulation are investigated. Methods and results The powder size distribution and composition of TBP are measured. The GIOP female mice induced by dexamethasone intramuscular injection are used to examine the anti‐osteoporosis effects of TBP in a 10 week experiment, and improved bone mineral density and bone microarchitecture are observed via micro‐CT. In addition, qRT‐PCR results show that the NF‐κB pathway is inhibited to reduce bone resorption, whereas the Wnt/β‐catenin pathway is activated to enhance bone formation after treatment. Moreover, TBP treatments suppress the release of pro‐inflammatory cytokines, repair dysfunction of the intestinal epithelial barrier, and prevent aggravated systemic inflammation in mRNA levels. Additionally, 16S rRNA gene sequencing indicate that TBP treatments enhance the abundance of anti‐inflammatory bacteria and short‐chain fatty acid (SCFA) producers, which is consistent with increased SCFA contents in feces measured via GC–MS. Conclusion These data show that TBP ameliorates GIOP in mice through four aspects, including coregulating signaling pathways, blocking proinflammatory cytokines, repairing the intestinal epithelial barrier, and modulating gut microbiota. Therefore, TBP may be a potential prebiotic agent to alleviate osteoporosis in humans.
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