ArticleCell biochemistry and biophysics2026
Diosmin-Hesperidin Combination Improves Post-Ischemic Cardiac Recovery Via AKT/mTORC1 Modulation in Doxorubicin-Treated Rats.
Article in Cell biochemistry and biophysics, 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
8 authors.
Funding
Abstract
Citrus fruits are rich in flavonoids, such as diosmin and hesperidin, which exhibit antioxidant properties. The combination of diosmin and hesperidin (DH) has shown potential cardiovascular benefits. Doxorubicin (DOX) is a chemotherapy drug known to cause cardiotoxicity. Hearts pre-treated with DOX show increased susceptibility to ischemia-reperfusion (I/R) damage. This study aimed to investigate the cardioprotective potential of DH against I/R injury in animal models with prior DOX exposure. Rats were divided into five groups: control group (normal saline); DOX group (2.5 mg/kg intraperitoneally, six times over two weeks); DOX + low-DH group (50 mg/kg/day orally for 14 days); DOX + high-DH group (100 mg/kg/day orally for 14 days); and DH group (100 mg/kg/day orally for 14 days). Following treatments, isolated hearts underwent global ischemia-reperfusion protocol with hemodynamic measurements recorded at baseline and post-reperfusion. DH pre-treatment significantly reduced DOX-associated cardiac injury, demonstrating protective effects both under baseline conditions and during post-ischemia recovery by improving LVDP and RPP, reducing coronary flow LDH levels, and mitigating histopathological damage (necrosis, degradation, and inflammation). Additionally, DH increased the cardiac GSH to GSSG ratio and enhanced GPx activity, while decreasing GSR activity. Furthermore, DH pretreatment down-regulated the overexpression of AKT, mTORC1, and ULK1 mRNA. Moreover, the molecular docking study demonstrated that Daflon’s active components (diosmin and hesperidin) counteract DOX-induced cardiotoxicity by dually inhibiting both AKT and mTORC1 expression. These findings demonstrated that DH protected against DOX-induced I/R damage via AKT/mTORC1 modulation.
Indexed as
Identifiers
41649666What 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.