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Protective effects of emodin against cisplatin‐induced oxidative stress in cultured human kidney (HEK 293) cells
Author(s) -
Waly Mostafa,
Ali Badreldin H,
Al-Lawati Intisar,
Nemmar A
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.823.9
Subject(s) - emodin , oxidative stress , glutathione , antioxidant , glutathione peroxidase , superoxide dismutase , pharmacology , chemistry , cisplatin , glutathione reductase , hek 293 cells , catalase , biochemistry , enzyme , biology , medicine , receptor , chemotherapy
Recent studies indicated that emodin 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 cells viability and restored the cisplatin‐induced glutathione (GSH) depletion and total antioxidant capacity (TAC) in a dose‐dependent manner. Emodin augmented the cisplatin‐induced inhibition of antioxidant enzymes [(catalase (CAT), glutathione peroxidase (GPx), glutathione S‐transferase (GST), glutathione reductase (GR) and superoxide dismutase (SOD)]. These results suggest that modin has the potential to be used as an adjunct therapeutic agent in patients receiving cisplatin treatment.