ArticleExperimental and therapeutic medicine2017
Areca nut extract protects against ovariectomy-induced osteoporosis in mice.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Biological Effects and Biomedical Applications of Areca Nut and Its Extract.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Antiosteoporosis effect of bryodulcosigenin on ovariectomy-induced osteoporosis in experimental rats.Acta cirurgica brasileira · 2024Article
- Comprehensive insights into areca nut: active components and omics technologies for bioactivity evaluation and quality control.Frontiers in pharmacology · 2024Review
- Betel Nut Chewing Decreased Calcaneus Ultrasound T-Score in a Large Taiwanese Population Follow-Up Study.Nutrients · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen deficiency increases the generation of reactive oxygen species (ROS), which is a crucial pathogenic factor for osteoporosis. Areca nuts are rich in phenolics, which have high antioxidant activity. In the present study, an ovariectomy (OVX)-induced osteoporosis mouse model was used to investigate the protective effects of areca nut extract (ANE) on bone loss and related processes. A total of 24 8-week-old female mice were randomly divided into three groups (n=8 per group): I Sham-operated control; II, bilateral OVX; and III, bilateral OVX + ANE. Group III were treated orally with ANE at a single dose of 300 mg/kg body weight daily for 6 months. ANE supplementation for 6 months improved trabecular bone microarchitecture and significantly increased bone mineral density in the distal femur (P<0.05) compared with Group II. Furthermore, serum levels of the osteoclast differentiation-inducing factors, receptor activator of nuclear factor-κB ligand and osteoprotegerin were significantly increased and decreased, respectively (both P<0.05), in OVX mice and these effects were significantly inhibited by ANE treatment (both P<0.05). ANE supplementation also resulted in significantly decreased serum hydrogen peroxide and malondialdehyde levels compared with Group II, while the levels of glutathione and catalase activity were significantly increased (P<0.05 and P<0.01, respectively). The current study indicated that the protective effects of ANE against bone loss were mediated, at least in part, via inhibition of the release of ROS and bone resorption. These results suggested that ANE could have therapeutic value in the treatment of osteoporosis.
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Registered trials
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