Aller au contenu principal
Accès ouvert déclaré2026article

The Molecular Mechanism of Eurycoma Longifolia in The Protection Against Osteoporosis in Orchidectomized Rats

0Citations signalées
1Institutions associées
1Pays d’affiliation

Résumé fourni par la source

Previous research on orchidectomized rats, a model for androgen-deficient osteoporosis, has demonstrated that Eurycoma longifolia (EL) protects against bone calcium loss. Although the exact mechanism is unknown, it might be connected to its capacity to raise testosterone levels or have a direct impact on bone remodeling. This study aims to determine the mechanism involved by investigating the effects of EL extract on gene expression of Receptor Activator of Nuclear Factor kappa-B ligand (RANKL), Osteoprotegerin (OPG), and Macrophage-Colony Stimulating Factor (MCSF) in orchidectomized rats. Thirty-two male Sprague-Dawley rats were divided into four groups of eight rats each, and each group received a different treatment for six weeks, namely the sham-operated group, the orchidectomized-control group, the orchidectomized group treated with EL (15 mg/kg), and the orchidectomized group treated with testosterone (8 mg/kg). Three genes were measured by dissecting the left and right tibia: RANKL (receptor activator of nuclear factor kappa B ligand), OPG (osteoprotegerin), and M-CSF (macrophage colony-stimulating factor). They were measured using the branched DNA technique (bDNA). For the expression of RANKL, OPG, and M-CSF, there was significant upregulation of OPG in the group of rats treated with Eurycoma Longifolia compared to the other group. In summary, supplementing the orchidectomized rats with EL extract upregulated OPG gene expression. These actions may be responsible for the protective effects of EL extract against bone resorption due to androgen deficiency.

Institutions

Sujets associés

Phytochemical compounds biological activitiesBone Metabolism and DiseasesBone health and osteoporosis research

BNTIC News n’est pas le producteur de ces données. Métadonnées interrogées à la demande auprès de OpenAlex (CC0). Sources et limites.