Jingjing Li1,2, Mingyuan Yang1,2, Chenyang Lu1,2, Jiaojiao Han1,2, Shasha Tang1,2, Jun Zhou1,2, Ye Li1,2, Tinghong Ming1,2, Zaijie Jim Wang3, Xiurong Su1,2. 1. State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Ningbo University, Ningbo, 315000, China. 2. School of Marine Science, Ningbo University, Ningbo, 315000, China. 3. Department of Biopharmaceutical Sciences, University of Illinois, Chicago, IL, 60612, USA.
Abstract
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.
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.