Key result
Diosmin attenuates doxorubicin-induced dilated cardiomyopathy in rats by modulating the Nrf2/TGF-β/PPAR-γ pathway.
Why the study?
The molecular mechanism and therapeutic potential of diosmin in doxorubicin-induced dilated cardiomyopathy remained to be explored.
Does diosmin improve doxorubicin-induced dilated cardiomyopathy in a rat model?
Population
Adult male Wistar rats divided into five groups (n = 8)
Comparison
Diosmin (25, 50, or 100 mg/kg/p.o.) with doxorubicin vs doxorubicin control and normal control
Design
Animal experimental study and molecular docking
Follow-up
28 days
Authors
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Hypothesis-generating for diosmin in doxorubicin cardiotoxicity; leaves open translation to human disease and clinical use.
Does diosmin improve doxorubicin-induced dilated cardiomyopathy in a rat model?
Diosmin demonstrates cardioprotective effects against doxorubicin-induced dilated cardiomyopathy in rats via modulation of the Nrf2/TGF-β/PPAR-γ pathway.
Jyoti et al. (2026) studied Doxorubicin-induced dilated cardiomyopathy (n=40). Diosmin vs. Normal control and doxorubicin control was evaluated on Cardiotoxicity assessed using oxidative, inflammatory and cardiac enzyme markers and histopathology. Diosmin treatment (25-100 mg/kg) significantly improved cardiac dysfunction and attenuated doxorubicin-induced dilated cardiomyopathy in rats by modulating the Nrf2/TGF-β/PPAR-γ pathway.
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