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Background <p>Cisplatin (CP) chemotherapy can elicit clinically meaningful cardiac injury, and the additional use of effective cardioprotective agents is a pressing need. This study investigated the protective effects and mechanisms of gastrodin against CP-induced cardiotoxicity, through redox-, inflammatory-, apoptotic-, and Nrf2-axis mechanisms.</p> Methods <p>Adult male Swiss albino mice received CP (5&#xa0;mg/kg, i.p., Days 3 and 6) with or without oral gastrodin (50 or 100&#xa0;mg/kg/day) for 7 days. Outcomes included cardiac histology, serum/tissue injury markers, myocardial ATP, oxidative stress indices, cytokines, and qRT-PCR for apoptosis- and Nrf2-pathway genes.</p> Results <p>CP produced marked myocardial injury, increasing the histological injury score (<i>p</i> &lt; 0.001), and elevated serum cTnI (<i>p</i> &lt; 0.001). CP depleted myocardial ATP (<i>p</i> &lt; 0.001) and increased lipid peroxidation, as reflected by elevated MDA (<i>p</i> &lt; 0.001). These changes were accompanied by increased TNF-α and IL-6 (<i>p</i> &lt; 0.001). Gastrodin 100&#xa0;mg/kg significantly attenuated these alterations, reducing the histological injury score, serum cTnI, restoring ATP, and lowering MDA (<i>p</i> &lt; 0.05–0.001 vs. CP). Gastrodin also reduced TNF-α and IL-6 and shifted gene expression toward cytoprotection.</p> Conclusion <p>Gastrodin may have a protective activity against CP cardiotoxicity, primarily by restoring redox balance/energy status, suppressing inflammation and apoptosis, and modulating p62–Keap1–Nrf2 related gene expression.</p>

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Gastrodin mitigates cisplatin-induced cardiotoxicity in Swiss albino mice by restoring redox homeostasis and modulating the p62–Keap1–Nrf2 Axis

  • 期刊论文

  • 发表日期：

    2026年7月20日

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  • Abdelrahim Alqudah,
  • Esam Qnais,
  • Yousra Bsieso,
  • Amjad E. Hamdallah,
  • Omar Gammoh,
  • Sireen Abdul Rahim Shilbayeh,
  • Alaa A. A. Aljabali

摘要

Background

Cisplatin (CP) chemotherapy can elicit clinically meaningful cardiac injury, and the additional use of effective cardioprotective agents is a pressing need. This study investigated the protective effects and mechanisms of gastrodin against CP-induced cardiotoxicity, through redox-, inflammatory-, apoptotic-, and Nrf2-axis mechanisms.

Methods

Adult male Swiss albino mice received CP (5 mg/kg, i.p., Days 3 and 6) with or without oral gastrodin (50 or 100 mg/kg/day) for 7 days. Outcomes included cardiac histology, serum/tissue injury markers, myocardial ATP, oxidative stress indices, cytokines, and qRT-PCR for apoptosis- and Nrf2-pathway genes.

Results

CP produced marked myocardial injury, increasing the histological injury score (p < 0.001), and elevated serum cTnI (p < 0.001). CP depleted myocardial ATP (p < 0.001) and increased lipid peroxidation, as reflected by elevated MDA (p < 0.001). These changes were accompanied by increased TNF-α and IL-6 (p < 0.001). Gastrodin 100 mg/kg significantly attenuated these alterations, reducing the histological injury score, serum cTnI, restoring ATP, and lowering MDA (p < 0.05–0.001 vs. CP). Gastrodin also reduced TNF-α and IL-6 and shifted gene expression toward cytoprotection.

Conclusion

Gastrodin may have a protective activity against CP cardiotoxicity, primarily by restoring redox balance/energy status, suppressing inflammation and apoptosis, and modulating p62–Keap1–Nrf2 related gene expression.