ArticleScientific reports2026
Oleuropein attenuates steroid-induced osteonecrosis of the femoral head by inhibiting osteoblast apoptosis via activation of the PI3K-AKT-Bcl2 pathway.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
teroid-induced osteonecrosis of the femoral head (SONFH) is a severe bone disorder caused by long-term glucocorticoid administration and is characterized by osteoblast apoptosis. Oleuropein (OLP), a natural compound with anti-inflammatory and antioxidant properties, has demonstrated anti-apoptotic potential in bone-related diseases. However, its therapeutic role in SONFH has not yet been elucidated. This study aimed to investigate the therapeutic effects of OLP on SONFH and elucidate its underlying molecular mechanisms. In vitro, MC3T3-E1 osteoblasts treated with methylprednisolone (MPS) were co-incubated with OLP. Cell viability was assessed using a CCK-8 assay and live/dead cell staining. In vivo, a rat SONFH model was established with lipopolysaccharide and MPS, followed by OLP treatment. Bone microstructure was analyzed by micro-computed tomography and histopathological staining (H&E, Masson, Goldner). Network pharmacology and proteomics analyses were used to identify key targets and pathways related to the effects of OLP on SONFH. Apoptosis was examined with flow cytometry, TUNEL staining and ELISA. Protein and mRNA expression levels of relevant targets and pathways were examined with western blotting and quantitative real-time polymerase chain reaction. OLP significantly reversed MPS-induced osteoblast apoptosis and enhanced cell viability. In SONFH rats, OLP reduced empty lacunae, restored trabecular bone structure, and improved collagen organization. Molecular docking confirmed OLP's binding to AKT and Bcl2. Network pharmacology and proteomics highlighted apoptosis regulation, PI3K-AKT signaling, and cell cycle control as key mechanisms. Furthermore, OLP activated the PI3K-AKT-Bcl2 pathway, increasing p-PI3K, p-AKT, and Bcl2 levels while decreasing Caspase3 and Caspase9. OLP also promoted osteogenesis (upregulated ALP and Runx2) and angiogenesis (increased vWF and CD31). OLP alleviates SONFH by inhibiting osteoblast apoptosis and promoting osteogenesis and angiogenesis through activation of the PI3K-AKT-Bcl2 pathway. These findings support OLP as a promising natural compound for early intervention in SONFH.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.