PDF(Pubmed)
Abstract：
UNASSIGNED: Osteoporosis (OP) is a systemic metabolic bone disease characterized by decreased bone mass and destruction of bone microstructure, which tends to result in enhanced bone fragility and related fractures. The postmenopausal osteoporosis (PMOP) has a relatively high proportion, and numerous studies reveal that estrogen-deficiency is related to the imbalance of gut microbiota (GM), impaired intestinal mucosal barrier function and enhanced inflammatory reactivity. However, the underlying mechanisms remain unclear and the existing interventions are also scarce.
UNASSIGNED: In this study, we established a mouse model induced by ovariectomy (OVX) and conducted fecal microbiota transplantation (FMT) by gavage every day for 8 weeks. Subsequently, the bone mass and microarchitecture of mice were evaluated by the micro computed tomography (Micro-CT). The intestinal permeability, pro-osteoclastogenic cytokines expression, osteogenic and osteoclastic activities were detected by the immunohistological analysis, histological examination, enzyme-linked immunosorbent assay (ELISA) and western blot analysis accordingly. Additionally, the composition and abundance of GM were assessed by 16S rRNA sequencing and the fecal short chain fatty acids (SCFAs) level was measured by metabolomics.
UNASSIGNED: Our results demonstrated that FMT inhibited the excessive osteoclastogenesis and prevented the OVX-induced bone loss. Specifically, compared with the OVX group, FMT enhanced the expressions of tight junction proteins (zonula occludens protein 1 (ZO-1) and Occludin) and suppressed the release of pro-osteoclastogenic cytokines (tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)). Furthermore, FMT also optimized the composition and abundance of GM, and increased the fecal SCFAs level (mainly acetic acid and propionic acid).
UNASSIGNED: Collectively, based on GM-bone axis, FMT prevented the OVX-induced bone loss by correcting the imbalance of GM, improving the SCFAs level, optimizing the intestinal permeability and suppressing the release of pro-osteoclastogenic cytokines, which may be an alternative option to serve as a promising candidate for the prevention and treatment of PMOP in the future.
UNASSIGNED: This study indicates the ingenious involvement of GM-bone axis in PMOP and the role of FMT in reshaping the status of GM and ameliorating the bone loss in OVX-induced mice. FMT might serve as a promising candidate for the prevention and treatment of PMOP in the future.
UNASSIGNED: In this study, we established a mouse model induced by ovariectomy (OVX) and conducted fecal microbiota transplantation (FMT) by gavage every day for 8 weeks. Subsequently, the bone mass and microarchitecture of mice were evaluated by the micro computed tomography (Micro-CT). The intestinal permeability, pro-osteoclastogenic cytokines expression, osteogenic and osteoclastic activities were detected by the immunohistological analysis, histological examination, enzyme-linked immunosorbent assay (ELISA) and western blot analysis accordingly. Additionally, the composition and abundance of GM were assessed by 16S rRNA sequencing and the fecal short chain fatty acids (SCFAs) level was measured by metabolomics.
UNASSIGNED: Our results demonstrated that FMT inhibited the excessive osteoclastogenesis and prevented the OVX-induced bone loss. Specifically, compared with the OVX group, FMT enhanced the expressions of tight junction proteins (zonula occludens protein 1 (ZO-1) and Occludin) and suppressed the release of pro-osteoclastogenic cytokines (tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)). Furthermore, FMT also optimized the composition and abundance of GM, and increased the fecal SCFAs level (mainly acetic acid and propionic acid).
UNASSIGNED: Collectively, based on GM-bone axis, FMT prevented the OVX-induced bone loss by correcting the imbalance of GM, improving the SCFAs level, optimizing the intestinal permeability and suppressing the release of pro-osteoclastogenic cytokines, which may be an alternative option to serve as a promising candidate for the prevention and treatment of PMOP in the future.
UNASSIGNED: This study indicates the ingenious involvement of GM-bone axis in PMOP and the role of FMT in reshaping the status of GM and ameliorating the bone loss in OVX-induced mice. FMT might serve as a promising candidate for the prevention and treatment of PMOP in the future.
摘要：
UNASSIGNED：骨质疏松症（OP）是一种全身性代谢性骨病，其特征是骨量减少和骨微结构破坏，这往往会导致骨脆性增强和相关的骨折。绝经后骨质疏松症(PMOP)占比较高,大量研究表明，雌激素缺乏与肠道微生物群(GM)失衡有关，肠粘膜屏障功能受损，炎症反应性增强。然而,潜在的机制仍不清楚,现有的干预措施也很少.
未经批准：在这项研究中，我们建立了卵巢切除术（OVX）诱导的小鼠模型，并通过每天灌胃进行粪便微生物移植（FMT），持续8周。随后，通过显微计算机断层扫描（Micro-CT）评估小鼠的骨量和微结构。肠道通透性，促破骨细胞细胞因子表达，通过免疫组织学分析检测成骨和破骨细胞活性，组织学检查,相应的酶联免疫吸附测定(ELISA)和蛋白质印迹分析。此外,通过16SrRNA测序评估GM的组成和丰度,并通过代谢组学测定粪便短链脂肪酸(SCFAs)水平.
UNASSIGNED：我们的结果表明FMT抑制了过度的破骨细胞生成并防止了OVX诱导的骨丢失。具体来说,与OVX组相比，FMT增强了紧密连接蛋白（闭合zonula蛋白1（ZO-1）和Occludin）的表达，并抑制了促破骨细胞细胞因子（肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β））的释放。此外，FMT还优化了GM的组成和丰度，并增加粪便SCFA水平（主要是乙酸和丙酸）。
未经批准：集体，基于GM-骨轴，FMT通过纠正GM的失衡来预防OVX引起的骨丢失，提高SCFA水平，优化肠道通透性和抑制促破骨细胞细胞因子的释放，这可能是一个替代选择，作为一个有希望的候选人在未来的PMOP的预防和治疗。
UNASSIGNED：这项研究表明GM-骨轴在PMOP中的巧妙参与以及FMT在重塑GM状态和改善OVX诱导的小鼠骨丢失中的作用。FMT可能成为未来PMOP预防和治疗的有希望的候选者。
未经批准：在这项研究中，我们建立了卵巢切除术（OVX）诱导的小鼠模型，并通过每天灌胃进行粪便微生物移植（FMT），持续8周。随后，通过显微计算机断层扫描（Micro-CT）评估小鼠的骨量和微结构。肠道通透性，促破骨细胞细胞因子表达，通过免疫组织学分析检测成骨和破骨细胞活性，组织学检查,相应的酶联免疫吸附测定(ELISA)和蛋白质印迹分析。此外,通过16SrRNA测序评估GM的组成和丰度,并通过代谢组学测定粪便短链脂肪酸(SCFAs)水平.
UNASSIGNED：我们的结果表明FMT抑制了过度的破骨细胞生成并防止了OVX诱导的骨丢失。具体来说,与OVX组相比，FMT增强了紧密连接蛋白（闭合zonula蛋白1（ZO-1）和Occludin）的表达，并抑制了促破骨细胞细胞因子（肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β））的释放。此外，FMT还优化了GM的组成和丰度，并增加粪便SCFA水平（主要是乙酸和丙酸）。
未经批准：集体，基于GM-骨轴，FMT通过纠正GM的失衡来预防OVX引起的骨丢失，提高SCFA水平，优化肠道通透性和抑制促破骨细胞细胞因子的释放，这可能是一个替代选择，作为一个有希望的候选人在未来的PMOP的预防和治疗。
UNASSIGNED：这项研究表明GM-骨轴在PMOP中的巧妙参与以及FMT在重塑GM状态和改善OVX诱导的小鼠骨丢失中的作用。FMT可能成为未来PMOP预防和治疗的有希望的候选者。
