Protective effects of emodin against cisplatin-induced oxidative stress in cultured human kidney (HEK 293) cells

Authors

  • Mostafa I. Waly,

    Corresponding author
    • Department of Food Sciences and Nutrition, College of Agricultural and Marine Sciences, Sultan Qaboos University, Muscat, Oman
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    • Mostafa I. Waly and Badreldin H. Ali made equal contribution to study design, interpretation of data, statistical analysis and drafting the manuscript. Intisar Al-Lawati was involved in conducting the experimental laboratory work. Abderrahim Nemmar conceptualized the use of emodin in cisplatin nephrotoxicity, critically revised the manuscript and wrote the Discussion section. All authors read and approved the final manuscript.
  • Badreldin H. Ali,

    1. Department of Pharmacology, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman
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  • Intisar Al-Lawati,

    1. Department of Pharmacology, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman
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  • Abderrahim Nemmar

    1. Department of Physiology, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE
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Correspondence to: M. I. Waly, Department of Food Science and Nutrition, College of Agricultural and Marine Sciences, Sultan Qaboos University, PO Box 34 Al- Khod, Postal code 123, Oman.

E-mail: waly.mostafa@gmail.com

ABSTRACT

Emodin (a rhubarb anthraquinone) has strong antioxidant and anticancer actions, and recent studies indicated that it reduces cellular oxidative stress induced by various insults and drugs. Cisplatin is an anticancer drug that is associated with nephrotoxicity and induces oxidative stress in cultured human kidney (HEK 293) cells. This study aimed to assess the in-vitro antioxidant properties of the emodin against cisplatin-induced oxidative stress in HEK 293 cells. Our study revealed that emodin acted as a potent free radical scavenger and provided nephroprotection against cisplatin-induced oxidative stress. Emodin as low as 0.5 µm did not decrease cell viability and restored the cisplatin-induced glutathione depletion and total antioxidant capacity in a dose-dependent manner. Emodin augmented the cisplatin-induced inhibition of antioxidant enzymes (catalase, glutathione peroxidase, glutathione S-transferase, glutathione reductase and superoxide dismutase). These results suggest that emodin has the potential to be used as an adjunct therapeutic agent in patients receiving cisplatin treatment. Copyright © 2012 John Wiley & Sons, Ltd.

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