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

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.

Nurturing longevity through natural compounds: Where do we stand, and where do we go?

“…Among the natural compounds, subjected to intensive evaluation of geroprotective potential are resveratrol (D. Park et al., 2016; N. Wang et al., 2019), naringin (P. Guo et al., 2022), naringenin (G. Chen et al., 2022), phlorizin (S. Park & Park, 2022), and ferulic acid (H. Li et al., 2021). Interestingly, the use of glucosamine as a supplement to alleviate osteoporosis progression has been associated with elevated osteoblast autophagy (W. Su et al., 2022). In some cases, supplements do not directly target autophagy to benefit health and lifespan.…”

Regulatory signaling pathways of osteoblast autophagy in periprosthetic osteolysis

“…Vitro studies prove that kaempferol enhances the mineralization ability of MC3T3-E1 cells by promoting autophagy (Kim et al, 2016). Vivo studies suggest that glucosamine induces osteoblast differentiation and mineralization by promoting autophagy, thereby improving the prognosis of osteoporotic mice (Su et al, 2022). However, other studies show that rapamycininduced autophagy significantly reduces the activity and mineralization of osteoblasts.…”

The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis

“… 42 Similarly, in the galactose-induced OBs senescence model, glucosamine can improve the apoptosis of osteoblasts by promoting autophagy. 43 However, in the context of hypoxia, OBs exhibit an elevation in the expression of cyclin-dependent kinase 8 (CDK8), and the overexpression of CDK8 has been found to induce both autophagy and apoptosis in this cellular setting. 44 …”

“…42 Similarly, in the galactose-induced OBs senescence model, glucosamine can improve the apoptosis of osteoblasts by promoting autophagy. 43 However, in the context of hypoxia, OBs exhibit an elevation in the expression of cyclin-dependent kinase 8 (CDK8), and the overexpression of CDK8 has been found to induce both autophagy and apoptosis in this cellular setting. 44 The Involvement of Autophagy in OCs OCs, derived primarily from hematopoietic progenitor cells of the monocyte-macrophage lineage, serve as the exclusive cells responsible for bone resorption within the human body.…”