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<p>Celastrol (CELA) is a naturally occurring pentacyclic nortriterpenoid quinone found in <i>Tripterygium wilfordii</i> with diverse pharmacological activities. A major and constrictive adverse effect of cisplatin (CIS) is ovarian insufficiency, which affects both the reproductive and non-reproductive health. Current study investigated the ability of CELA to protect against CIS-induced ovarian toxicity in rats. Animals received CELA (0.5 and 1&#xa0;mg/kg; orally) for 17 consecutive days and CIS (6.0&#xa0;mg/kg; i.p.) on the 7th and 14th day of the study. CIS induced overt ovarian toxicity as indicated biochemically and histopathologically. CELA protected against CIS-induced reduction in the relative ovarian weight and serum levels of estradiol and anti-mullerian hormones. Co-treatment with CELA prevented the histopathological alterations in ovarian tissues and enhanced the fraction of healthy follicles. Further, it significantly ameliorated CIS-induced lipid peroxidation &amp; antioxidant enzyme exhaustion and inhibited the rise in the expression of the inflammatory markers; tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide synthase, and nuclear factor kappa B. This was associated with modulation of Bax and Bcl-2 mRNA expression in favor of inhibition of apoptosis. Notably, co-treatment with CELA prevented CIS-induced reduction in both peroxisome proliferators–activated receptor-γ (PPAR-γ) and phospho-AMP-activated protein kinase (p-AMPK) content. In conclusion, CELA protects against CIS-induced ovarian toxicity in rats. This may be attributed, at least partly, to its antioxidant, anti-inflammatory, and anti-apoptotic activities in addition to enhancement of PPAR-γ and p-AMPK expression in ovarian tissues.</p>

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Celastrol protects against cisplatin-induced ovarian toxicity via modulation of PPAR-γ and AMPK

  • 期刊论文

  • 发表日期：

    2025年6月7日

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  • Nabil A. Alhakamy,
  • Abdulmohsin J. Alamoudi,
  • Wesam H. Abdulaal,
  • Hani Choudhry,
  • Hani Z. Asfour,
  • Mohammed Wanees Al-Rabia,
  • Osama M. Ashour,
  • Ashraf B. Abdel-Naim,
  • Amal Hofni,
  • Esam M. Aboubakr

摘要

Celastrol (CELA) is a naturally occurring pentacyclic nortriterpenoid quinone found in Tripterygium wilfordii with diverse pharmacological activities. A major and constrictive adverse effect of cisplatin (CIS) is ovarian insufficiency, which affects both the reproductive and non-reproductive health. Current study investigated the ability of CELA to protect against CIS-induced ovarian toxicity in rats. Animals received CELA (0.5 and 1 mg/kg; orally) for 17 consecutive days and CIS (6.0 mg/kg; i.p.) on the 7th and 14th day of the study. CIS induced overt ovarian toxicity as indicated biochemically and histopathologically. CELA protected against CIS-induced reduction in the relative ovarian weight and serum levels of estradiol and anti-mullerian hormones. Co-treatment with CELA prevented the histopathological alterations in ovarian tissues and enhanced the fraction of healthy follicles. Further, it significantly ameliorated CIS-induced lipid peroxidation & antioxidant enzyme exhaustion and inhibited the rise in the expression of the inflammatory markers; tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide synthase, and nuclear factor kappa B. This was associated with modulation of Bax and Bcl-2 mRNA expression in favor of inhibition of apoptosis. Notably, co-treatment with CELA prevented CIS-induced reduction in both peroxisome proliferators–activated receptor-γ (PPAR-γ) and phospho-AMP-activated protein kinase (p-AMPK) content. In conclusion, CELA protects against CIS-induced ovarian toxicity in rats. This may be attributed, at least partly, to its antioxidant, anti-inflammatory, and anti-apoptotic activities in addition to enhancement of PPAR-γ and p-AMPK expression in ovarian tissues.