Cycloastragenol prevents age-related bone loss: Evidence in d-galactose-treated and aged rats

Yu, Yongjie; Wu, Jiahuan; Li, Jin; Liu, Yanzhi; Zheng, Xiaoyan; Du, Mingzhu; Zhou, Limin; Yang, Yajun; Luo, Sheng; Hu, Wenjia; Li, Lin; Yao, Weimin; Liu, Yuyu

doi:10.1016/j.biopha.2020.110304

Cited by 23 publications

(14 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results of micro-CT and bone biomechanics showed that bone mass, bone microstructure and biomechanical properties were significantly reduced in the modeling group. This was consistent with previously reported results [ 39 , 40 ]. To further verify whether d -Gal could accelerate aging, we detected the changes of serum SOD, MDA, IL-1β, IL-6 and other senescence related indexes [ 41 ].…”

Section: Discussionsupporting

confidence: 94%

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

Huang

Zheng

et al. 2022

Nutr Metab (Lond)

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 94%

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

Huang

Zheng

et al. 2022

Nutr Metab (Lond)

View full text Add to dashboard Cite

show abstract

“…The results of micro-CT and bone biomechanics showed that bone mass, bone microstructure and biomechanical properties were signi cantly reduced in the modeling group. This was consistent with previously reported results [39,40]. To further verify whether D-Gal could accelerate aging, we detected the changes of serum SOD, MDA, IL-1β, IL-6 and other senescence related indexes [41].…”

Section: Discussionsupporting

confidence: 91%

Glucosamine Delays the Progression of Osteoporosis in Senile Mice by Promoting Osteoblast Autophagy

Huang

Zheng

et al. 2022

Preprint

View full text Add to dashboard Cite

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.

show abstract

“…We also found that the change in Tb.Th was exhibited later than any other parameters. This finding was consistent with previous studies demonstrating that Tb.Th was a bone parameter which seldom changed in response to osteoporotic progression 5 , 45 . Although there were significant changes in bone histomorphometric parameters (BV/TV, Tb.N and Tb,Th) after either D-gal administration or HFD consumption, the levels of CTX-I were significantly increased only in some groups of animals without any changes in P1NP levels.…”

Section: Discussionmentioning

confidence: 99%

D-galactose-induced aging aggravates obesity-induced bone dyshomeostasis

Imerb

Thonusin

Pratchayasakul

et al. 2022

Sci Rep

View full text Add to dashboard Cite

We aimed to compare the time-course effect of D-galactose (D-gal)-induced aging, obesity, and their combined effects on bone homeostasis. Male Wistar rats were fed with either a normal diet (ND; n = 24) or a high-fat diet (HFD; n = 24) for 12 weeks. All rats were then injected with either vehicle or 150 mg/kg/day of D-gal for 4 or 8 weeks. Blood was collected to measure metabolic, aging, oxidative stress, and bone turnover parameters. Bone oxidative stress and inflammatory markers, as well as bone histomorphometry were also evaluated. Additionally, RAW 264.7 cells were incubated with either D-gal, insulin, or D-gal plus insulin to identify osteoclast differentiation capacity under the stimulation of receptor activator of nuclear factor κB ligand. At week 4, D-gal-induced aging significantly elevated serum malondialdehyde level and decreased trabecular thickness in ND- and HFD-fed rats, when compared to the control group. At week 8, D-gal-induced aging further elevated advanced glycation end products, increased bone inflammation and resorption, and significantly impaired bone microarchitecture in HFD-fed rats. The osteoclast number in vitro were increased in the D-gal, insulin, and combined groups to a similar extent. These findings suggest that aging aggravates bone dyshomeostasis in the obese condition in a time-dependent manner.

show abstract

Cycloastragenol prevents age-related bone loss: Evidence in d-galactose-treated and aged rats

Cited by 23 publications

References 41 publications

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

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

Glucosamine Delays the Progression of Osteoporosis in Senile Mice by Promoting Osteoblast Autophagy

D-galactose-induced aging aggravates obesity-induced bone dyshomeostasis

Contact Info

Product

Resources

About