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<p>The objective of this study is to explore the molecular mechanism and therapeutic potential of diosmin using both molecular docking and experimental methodologies in a rat model of doxorubicin-induced dilated cardiomyopathy. Adult male Wistar rats were divided into five groups (<i>n</i> = 8): normal control, doxorubicin control, doxorubicin + diosmin (25&#xa0;mg/kg/p.o.), doxorubicin + diosmin (50&#xa0;mg/kg/p.o.), and doxorubicin + diosmin (100&#xa0;mg/kg/p.o.) for 28&#xa0;days. Cardiotoxicity was assessed using oxidative, inflammatory and cardiac enzyme markers as well as a histopathological study. Doxorubicin causes ventricular dilation, increases oxidative stress by increases TBARS and depleting SOD levels, also reduces GSH and catalase levels, increases TNFα levels, and elevates cardiac enzyme markers such as CK-MB, calcium, TGF-β, and PPAR-γ. Diosmin treatment at various doses significantly improved cardiac dysfunction by decreasing oxidative stress, inflammatory cytokines, and elevated cardiac enzymes, while increasing Nrf2 and PPAR-γ and lowering TGF-β level. It is also near-normalised cardiac hypertrophy and fibrosis on histology. Interestingly, the <i>in silico</i> results strongly support biochemical investigation by examining diosmin binding affinities for Nrf2/TGF-β/PPAR-γ. The study suggests that Diosmin has antioxidant, anti-inflammatory and anti-apoptotic effects, improves cardiac remodelling and provides cardioprotection by modulating the Nrf2/TGF-β/PPAR-γ pathway, thereby enhancing antioxidant and cardiac enzyme levels and decreasing pro-inflammatory cytokines in cardiac cells, thereby attenuating doxorubicin-induced dilated cardiomyopathy.</p> Graphical abstract <p></p>

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Cardioprotective effects of diosmin against doxorubicin-induced dilated cardiomyopathy via Nrf2/TGF-β/PPAR-γ

  • 期刊论文

  • 发表日期：

    2026年5月23日

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  • Uma Jyoti,
  • Aman Thakur,
  • Sushma Devi

摘要

The objective of this study is to explore the molecular mechanism and therapeutic potential of diosmin using both molecular docking and experimental methodologies in a rat model of doxorubicin-induced dilated cardiomyopathy. Adult male Wistar rats were divided into five groups (n = 8): normal control, doxorubicin control, doxorubicin + diosmin (25 mg/kg/p.o.), doxorubicin + diosmin (50 mg/kg/p.o.), and doxorubicin + diosmin (100 mg/kg/p.o.) for 28 days. Cardiotoxicity was assessed using oxidative, inflammatory and cardiac enzyme markers as well as a histopathological study. Doxorubicin causes ventricular dilation, increases oxidative stress by increases TBARS and depleting SOD levels, also reduces GSH and catalase levels, increases TNFα levels, and elevates cardiac enzyme markers such as CK-MB, calcium, TGF-β, and PPAR-γ. Diosmin treatment at various doses significantly improved cardiac dysfunction by decreasing oxidative stress, inflammatory cytokines, and elevated cardiac enzymes, while increasing Nrf2 and PPAR-γ and lowering TGF-β level. It is also near-normalised cardiac hypertrophy and fibrosis on histology. Interestingly, the in silico results strongly support biochemical investigation by examining diosmin binding affinities for Nrf2/TGF-β/PPAR-γ. The study suggests that Diosmin has antioxidant, anti-inflammatory and anti-apoptotic effects, improves cardiac remodelling and provides cardioprotection by modulating the Nrf2/TGF-β/PPAR-γ pathway, thereby enhancing antioxidant and cardiac enzyme levels and decreasing pro-inflammatory cytokines in cardiac cells, thereby attenuating doxorubicin-induced dilated cardiomyopathy.

Graphical abstract