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Purpose <p>Diclofenac (DICL) is commonly prescribed for its anti-inflammatory and analgesic properties; however, its prolonged use can lead to significant liver and kidney damage due to oxidative stress. Natural antioxidants derived from plant sources, such as onion (<i>Allium cepa</i> L.) peel extract (ACPE), have gained attention for their potential to alleviate drug-induced organ toxicity. The purpose of this study was to assess the ameliorative influences of ACPE on DICL-induced hepato-nephrotoxicity in rats.</p> Methods <p>Twenty-four rats were segregated into four groups (6 rats for each group): Group I (healthy control); Group II received ACPE only (200&#xa0;mg/kg/day) for 10 consecutive days by oral gavage; Group III received DICL only (50&#xa0;mg/kg/day) for 3 consecutive days (days 8–10 of the experimental period) orally; and Group IV received ACPE (200&#xa0;mg/kg/day) for 10 days by oral gavage + DICL (50&#xa0;mg/kg/day) on the 8th, 9th, and 10th days.</p> Results <p>ACPE succeeded in attenuating the DICL-induced hepato- and nephrotoxicity; as evidenced by the remarkable reduction in serum creatinine, and urea (<i>P</i> &lt; 0.001). Liver function tests showed significant differences in serum ALT, AST, and albumin levels among the four groups (<i>P</i> = 0.004, 0.032, and 0.014, respectively), as well as decreased hepatic and renal cortical MDA and increased catalase activity (<i>P</i> &lt; 0.001). Moreover, ACPE downregulated cyclooxygenase-2 and upregulated <i>Nrf-2</i> gene expressions (<i>P</i> &lt; 0.001). ACPE effectively improved the histopathological changes of DICL toxicity on both the liver and kidney tissues.</p> Conclusion <p>Overall, our results highlighted that ACPE could represent a protective food supplement against oxidative stress and inflammatory abnormalities associated with DICL-induced hepato- and nephrotoxicity.</p>

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Mechanistic insights into the protective effects of red onion peel extract (Allium Cepa L.) against diclofenac-induced oxidative and inflammatory hepato-renal damage

  • 期刊论文

  • 发表日期：

    2026年3月9日

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  • Maha O. Hammad,
  • Sahar Ibrahem,
  • Osama Elsayed,
  • Rawan Mansoup,
  • Abdelrahman Allam,
  • Merna Mahmoud,
  • Mohamed Elkhedr,
  • Mayada Rashad,
  • Maryam Abdelmobdy,
  • MennaAllah Elnabawy,
  • Nadia Aboaish,
  • Mohammed. H. Abd El-Aziz

摘要

Purpose

Diclofenac (DICL) is commonly prescribed for its anti-inflammatory and analgesic properties; however, its prolonged use can lead to significant liver and kidney damage due to oxidative stress. Natural antioxidants derived from plant sources, such as onion (Allium cepa L.) peel extract (ACPE), have gained attention for their potential to alleviate drug-induced organ toxicity. The purpose of this study was to assess the ameliorative influences of ACPE on DICL-induced hepato-nephrotoxicity in rats.

Methods

Twenty-four rats were segregated into four groups (6 rats for each group): Group I (healthy control); Group II received ACPE only (200 mg/kg/day) for 10 consecutive days by oral gavage; Group III received DICL only (50 mg/kg/day) for 3 consecutive days (days 8–10 of the experimental period) orally; and Group IV received ACPE (200 mg/kg/day) for 10 days by oral gavage + DICL (50 mg/kg/day) on the 8th, 9th, and 10th days.

Results

ACPE succeeded in attenuating the DICL-induced hepato- and nephrotoxicity; as evidenced by the remarkable reduction in serum creatinine, and urea (P < 0.001). Liver function tests showed significant differences in serum ALT, AST, and albumin levels among the four groups (P = 0.004, 0.032, and 0.014, respectively), as well as decreased hepatic and renal cortical MDA and increased catalase activity (P < 0.001). Moreover, ACPE downregulated cyclooxygenase-2 and upregulated Nrf-2 gene expressions (P < 0.001). ACPE effectively improved the histopathological changes of DICL toxicity on both the liver and kidney tissues.

Conclusion

Overall, our results highlighted that ACPE could represent a protective food supplement against oxidative stress and inflammatory abnormalities associated with DICL-induced hepato- and nephrotoxicity.