ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Naringenin ameliorates postmenopausal osteoporosis by inhibiting BMSC oxidative stress via the PI3K/AKT/NRF2 pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Oxidative stress plays a critical role in the pathogenesis of various bone diseases, particularly osteoporosis. Naringenin, a small molecule compound confirmed to possess antioxidative stress properties, exerts anti-inflammatory effects in multiple diseases and can ameliorate osteoporotic symptoms. However, the precise mechanism by which Naringenin treats osteoporosis remains unclear. This study investigates the mechanism by which Naringenin inhibits oxidative stress in Bone Marrow Mesenchymal Stem Cells (BMSCs) to treat postmenopausal osteoporosis (PMOP). A mouse model of postmenopausal osteoporosis (PMOP) was established by ovariectomy (OVX). Micro-computed tomography (micro-CT) and histological staining were used to evaluate the therapeutic efficacy of naringenin against PMOP. Network pharmacology and molecular docking were applied to explore the underlying mechanism of naringenin in the treatment of PMOP. Cell counting kit-8 (CCK-8) assay, alkaline phosphatase (ALP) staining, Alizarin Red S (ARS) staining, Western blot and immunofluorescence staining were performed to investigate the effects and mechanisms of naringenin on relieving oxidative stress in bone marrow mesenchymal stem cells (BMSCs) and ameliorating PMOP. Naringenin alleviated bone loss caused by postmenopausal osteoporosis and upregulated the expression of BCL-2, RUNX2 and NRF2 in BMSCs within bone tissues. In the hydrogen peroxide (H
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