ArticleBiological trace element research2026
Vanadyl Acetylacetonate and Berberine Synergistically Ameliorate Diabetes-induced Vascular Dysfunction and Reduce Endothelial Toxicity through ERK and Akt Regulation.
Article in Biological trace element research, 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
10 authors.
Funding
Abstract
Vanadyl acetylacetonate (VO) and berberine (BBR) have both demonstrated anti-diabetic effects. Previous studies in type 1 diabetic rats suggest that their co-administration of VO and BBR is safer and more effective than either compound alone. However, the precise vascular effects and underlying molecular mechanisms remain unclear. Diabetic rats received VO, BBR, or both. Blood glucose and body weight were monitored. Alizarin Red staining detected vascular calcification. Vascular morphology, intercellular junctions (E-Cadherin/β-catenin staining), cytoskeleton (Phalloidin), and permeability (FITC-BSA) were assessed. Cell viability was evaluated via MTT assay, apoptosis kit, and flow cytometry. Western blotting analyzed Bax, Bcl-2, and related pathway proteins. NOS activity including tNOS and iNOS were measured. GO and KEGG pathway enrichment identified potential mechanisms. Co-administration of VO and BBR reduced blood glucose without affecting weight. It attenuated vascular calcification, preserved intercellular junctions, and improved endothelial barrier function. BBR reversed VO-induced E-Cadherin/β-catenin disruption, cytoskeletal damage, and permeability increase. Cell apoptosis reduced with BBR, associated with downregulation of Bax, upregulation of Bcl-2, and normalized tNOS and iNOS activity. Mechanistically, ERK and PI3K-Akt pathways were implicated. BBR suppressed VO-induced overactivation of p-ERK and p-Akt. VO and BBR synergistically improve glucose control and provide enhanced vascular protection more effectively than either compound alone in diabetic rats. Furthermore, BBR prevents the over-activation of ERK and Akt induced by VO, thereby reducing iNOS and tNOS production, subsequent apoptosis, intercellular junction damage, and increased permeability in HUVECs. These preliminary findings lay the groundwork for future research aimed at developing novel therapeutic strategies and safer anti-diabetic treatments with improved efficacy and reduced toxicity.
Indexed as
Identifiers
40775562What Socratic 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 Socratic graph.