ArticleOxidative medicine and cellular longevity2019
Curculigoside Protects against Excess-Iron-Induced Bone Loss by Attenuating Akt-FoxO1-Dependent Oxidative Damage to Mice and Osteoblastic MC3T3-E1 Cells.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 62 citations in OpenAlex.
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- The Therapeutic Effect of Natural Compounds on Osteoporosis through Ferroptosis.Current medicinal chemistry · 2024Review
- Cytoprotective Effect of Gallic Acid against Injuries Promoted by Therapeutic Ionizing Radiation in Preosteoblast Cells.International journal of molecular and cellular medicine · 2024Article
- Identification and experimental validation of programmed cell death- and mitochondria-associated biomarkers in osteoporosis and immune microenvironment.Frontiers in genetics · 2024Article
- Prevention and treatment of osteoporosis with natural products: Regulatory mechanism based on cell ferroptosis.Journal of orthopaedic surgery and research · 2023Review
- Curculigoside attenuates osteoporosis through regulating DNMT1 mediated osteoblast activity.In vitro cellular & developmental biology. Animal · 2023Article
- Phytochemical composition, antioxidant, in vitro and in silico studies of active compounds ofSaudi journal of biological sciences · 2023Article
- Anti-inflammatory and antioxidant traditional Chinese Medicine in treatment and prevention of osteoporosis.Frontiers in pharmacology · 2023Review
- Mechanism and Prospect of Gastrodin in Osteoporosis, Bone Regeneration, and Osseointegration.Pharmaceuticals (Basel, Switzerland) · 2022Review
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8 authors at 5 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
summaryThe present investigation found that curculigoside (CUR) can prevent excess-iron-induced bone loss in mice and cells through antioxidation and inhibiting excess-iron-induced phosphorylation of the Akt-FoxO1 pathway. CUR can attenuate the decreasing of cell viability, enhance autophagy, potentiate the antioxidant effect, and reduce apoptosis in MC3T3-E1 cells treated with excess iron through regulating the expression of FoxO1 target gene.
introductionOxidative stress induced by iron overload is an important factor involved in primary osteoporosis disease and iron overload-related diseases. Curculigoside (CUR), a phenolic glycoside found abundantly in
methodsAn iron-overload mice model was used to study the protective effects of CUR on bone loss induced by oxidative stress. Serum bone metabolism markers and antioxidant enzymes were also measured. To explore the antioxidant mechanism of CUR, the MC3T3-E1 osteoblastic cell line was used.
resultsIn vivo studies showed that BMD and microarchitectural parameters were improved after a 3-month administration of CUR. CUR improved the biochemical parameters related to bone metabolism and the expressions of Runx2, OCN, and type 1 collagen and increased the formation of bone-mineralized nodules
conclusionsThese results demonstrated that CUR was able to alleviate bone loss induced by oxidative stress resulting from iron overload, suggesting its potential use for the treatment of primary osteoporosis and bone loss in iron-overload-related diseases.
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