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Modulation of inflammatory, oxidative, and apoptotic stresses mediates the renoprotective effect of daidzein against glycerol-induced acute kidney injury in rats

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Abstract

Acute kidney injury (AKI) is a life-threatening complication that accompanies rhabdomyolysis. Daidzein is a dietary isoflavone that has various biological activities. This study examined the therapeutic potential of daidzein and the underlying mechanisms against AKI induced by glycerol in male rats. Animals were injected once with glycerol (50%, 10 ml/kg, intramuscular) for induction of AKI and pre-treated orally with daidzein (25, 50, and 100 mg/kg) for 2 weeks. Biochemical, histopathological, immunohistopathological, and molecular parameters were assessed to evaluate the effect of daidzein. The results revealed that the model group displayed remarkable functional, molecular, and structural changes in the kidney. However, pre-administration of daidzein markedly decreased the kidney relative weight as well as the levels of urea, creatinine, K, P, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and cystatin C. Further, daidzein lessened the rhabdomyolysis-related markers [lactate dehydrogenase (LDH) and creatine kinase (CK)]. Notably, the enhancement of the antioxidant biomarkers [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and reduced glutathione (GSH) is accompanied by a decrease in malondialdehyde (MDA) and nitric oxide (NO) levels. Moreover, upregulated gene expression levels of nuclear factor erythroid 2-related factor 2 (Nfe212) and hemeoxygenase-1 (Hmox1) were exerted by daidzein administration. Rats who received daidzein displayed markedly lower interleukin-1β (IL-1β), tumor nuclear factor-α (TNF-α), myleoperoxidase (MPO), and nuclear factor kappa B (NF-κB) levels together with higher interleukin-10 (IL-10) related to the model group. Remarkably, significant declines were noticed in the pro-apoptotic (Bax and caspase-3) and rises in antiapoptotic (Bcl-2) levels in the group that received daidzein. The renal histological screening validated the aforementioned biochemical and molecular alterations. Our findings support daidzein as a potential therapeutic approach against AKI-induced renal injury via suppression of muscle degradation, oxidative damage, cytokine release, and apoptosis.

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Acknowledgements

The authors thank the Taif University Researchers Supporting Program (Project number: TURSP-2020/151), Taif University, Saudi Arabia, for supporting the current study.

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Authors and Affiliations

  1. Department of Zoology and Entomology, Faculty of Science, Helwan University, Ain Helwan, 11795, Egypt

    Rami B. Kassab, Ahmed E. Abdel Moneim & Ahmed A. Moustafa

  2. Department of Biology, Faculty of Science and Arts, Al-Baha University, Almakhwah, Al-Baha, Saudi Arabia

    Rami B. Kassab, Hussam A. Althagafi & Ali O. Al-Ghamdy

  3. Chemistry Department, Faculty of Science, Al-Azhar University (Boys’ Branch), Nasr City, Cairo, Egypt

    Ahmed A. Elhenawy

  4. Department of Laboratory Medicine, Security Forces Hospital, Mecca, Saudi Arabia

    AbdulrahmanTheyab

  5. Research Center, King Faisal Specialist Hospital and Research Center, MBC-J04, P.O. Box 40047, Jeddah, 21499, Saudi Arabia

    Yousef M. Hawsawi

  6. Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, University of Tabuk, Tabuk, Saudi Arabia

    Osama M. Al-Amer

  7. Department of Biology, Genome and Biotechnology Unit, Faculty of Sciences, University of Tabuk, Tabuk, Saudi Arabia

    Atif Abdulwahab A. Oyouni

  8. Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, Egypt

    Ola A. Habotta

  9. Department of Biology, College of Science, Taif University, Taif, Saudi Arabia

    Fahad Alharthi

  10. Biology Department, College of Science and Humanities, Prince Sattam bin Abdul Aziz University, Alkharj, Saudi Arabia

    Maha S. Lokman

  11. Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, P.O. Box 11099, Taif, 21944, Saudi Arabia

    Khalaf F. Alsharif

  12. Department of Human Anatomy, College of Medicine, Taif University, P.O. Box 11099, Taif, 21944, Saudi Arabia

    Ashraf Albrakati

  13. Department of Zoonoses, Faculty of Veterinary Medicine, Sohag University, Sohag, 82524, Egypt

    Ehab Kotb Elmahallawy

  14. Departamento de Sanidad Animal, Grupo de Investigación en Sanidad Animal y Zoonosis (GISAZ), Facultad de Veterinaria, Universidad de Córdoba, Córdoba, Spain

    Ehab Kotb Elmahallawy

  15. Department of Cancer and Molecular Biology, National Cancer Institute, Cairo University, Cairo, Egypt

    Mohamed A. Elhefny

  16. Department of Medical Genetics, Faculty of Medicine, Umm Al-Qura University, Alqunfudah, Saudi Arabia

    Mohamed A. Elhefny

  17. Pathology Department, College of Medicine, Taif University, P.O. Box 11099, Taif, 21944, Saudi Arabia

    Kalid E. Hassan

  18. Surgery Department, College of Medicine, Al-Qunfudah Branch, Umm Al-Qura University, Makkah, Saudi Arabia

    Alaa Jameel A. Albarakati

  19. Urology Department, Tulane University, 1430 Tulane Avenue, New Orleans, LA, 70112, USA

    Ahmed A. Moustafa

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  1. Rami B. Kassab
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  18. Ahmed E. Abdel Moneim
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  19. Ahmed A. Moustafa
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Contributions

All authors were involved in the conception of the idea, performed data analysis and interpretation, provided resources, were responsible for data curation, wrote and edited the manuscript, and reviewed drafts of the paper. All authors read and approved the final version of the manuscript.

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Correspondence to Ehab Kotb Elmahallawy.

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All experimental procedures were accepted by the department of zoology and entomology, faculty of science, Helwan University (Cairo, Egypt; approval no, HU2021/Z/RKA0921-01).

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Kassab, .B., Elhenawy, A.A., AbdulrahmanTheyab et al. Modulation of inflammatory, oxidative, and apoptotic stresses mediates the renoprotective effect of daidzein against glycerol-induced acute kidney injury in rats. Environ Sci Pollut Res 30, 119016–119033 (2023). https://doi.org/10.1007/s11356-023-30461-4

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  • DOI: https://doi.org/10.1007/s11356-023-30461-4

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