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氨基葡萄糖通过促进成骨细胞自噬延缓老年小鼠骨质疏松症的进展。

Glucosamine delays the progression of osteoporosis in senile mice by promoting osteoblast autophagy.

作者信息

Su Wei, Lv Chen, Huang Lingtuo, Zheng XiaoHang, Yang Shengwu

机构信息

Department of Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.

出版信息

Nutr Metab (Lond). 2022 Nov 8;19(1):75. doi: 10.1186/s12986-022-00688-y.

DOI:10.1186/s12986-022-00688-y
PMID:36348458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9641921/
Abstract

BACKGROUND

Senile osteoporosis (SOP) is one of the most prevalent diseases that afflict the elderly population, which characterized by decreased osteogenic ability. Glucosamine (GlcN) is an over-the-counter dietary supplement. Our previous study reported that GlcN promotes osteoblast proliferation by activating autophagy in vitro. The purpose of this study is to determine the effects and mechanisms of GlcN on senile osteoporosis and osteogenic differentiation in vivo.

METHODS

Aging was induced by subcutaneous injection of D-Galactose (D-Gal), and treated with GlcN or vehicle. The anti-senile-osteoporosis effect of GlcN was explored by examining changes in micro-CT, serum indicators, body weight, protein and gene expression of aging and apoptosis. Additionally, the effects of GlcN on protein and gene expression of osteogenesis and autophagy were observed by inhibiting autophagy with 3-methyladenine (3-MA).

RESULTS

GlcN significantly improved bone mineral density (BMD) and bone micro-architecture, decreased skeletal senescence and apoptosis and increased osteogenesis in D-Gal induced osteoporotic mice. While all effect was reversed with 3-MA.

CONCLUSION

GlcN effectively delayed the progression of osteoporosis in senile osteoporotic mice by promoting osteoblast autophagy. This study suggested that GlcN may be a prospective candidate drug for the treatment of SOP.

摘要

背景

老年性骨质疏松症(SOP)是困扰老年人群的最常见疾病之一,其特征是成骨能力下降。氨基葡萄糖(GlcN)是一种非处方膳食补充剂。我们之前的研究报道,GlcN在体外通过激活自噬促进成骨细胞增殖。本研究的目的是确定GlcN在体内对老年性骨质疏松症和成骨分化的影响及机制。

方法

通过皮下注射D-半乳糖(D-Gal)诱导衰老,并给予GlcN或溶剂处理。通过检测微型计算机断层扫描(micro-CT)、血清指标、体重、衰老和凋亡相关蛋白及基因表达的变化,探讨GlcN的抗老年性骨质疏松症作用。此外,用3-甲基腺嘌呤(3-MA)抑制自噬,观察GlcN对成骨和自噬相关蛋白及基因表达的影响。

结果

GlcN显著提高了D-Gal诱导的骨质疏松小鼠的骨密度(BMD)和骨微结构,降低了骨骼衰老和凋亡,增加了成骨。而3-MA使所有这些作用均逆转。

结论

GlcN通过促进成骨细胞自噬有效延缓了老年性骨质疏松小鼠骨质疏松的进展。本研究提示GlcN可能是治疗SOP的一种有前景的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/7c3e48d1a4be/12986_2022_688_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/7e3f23323871/12986_2022_688_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/217b6383c2e2/12986_2022_688_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/e42b771920fa/12986_2022_688_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/f79214953163/12986_2022_688_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/d550aa1603c4/12986_2022_688_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/7c3e48d1a4be/12986_2022_688_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/7e3f23323871/12986_2022_688_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/217b6383c2e2/12986_2022_688_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/e42b771920fa/12986_2022_688_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/f79214953163/12986_2022_688_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/d550aa1603c4/12986_2022_688_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7e1/9641921/7c3e48d1a4be/12986_2022_688_Fig6_HTML.jpg

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