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Cannabidiol attenuates cisplatin‐induced nephrotoxicity by decreasing oxidative/nitrosative stress, inflammation and cell death
Author(s) -
Pacher Pal,
Mukhopadhyay Partha,
Pan Hao,
Rajesh Mohanraj,
Patel Vivek,
Mukhopadhyay Bani,
Becker Lauren,
Bátkai Sandor,
Gao Bin,
Haskó György
Publication year - 2009
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.23.1_supplement.617.5
Subject(s) - cannabidiol , cisplatin , nephrotoxicity , pharmacology , oxidative stress , nitrotyrosine , medicine , inflammation , chemotherapy , kidney , cancer research , immunology , nitric oxide , nitric oxide synthase , cannabis , psychiatry
The platinum compound cisplatin is one of the most potent chemotherapy agents available to treat various malignancies. Nephrotoxicity is a common complication of cisplatin chemotherapy, which involves increased oxidative and nitrosative stress, limiting its clinical use. In this study we have investigated the effects of a nonpsychoactive cannabinoid cannabidiol, which was reported to exert antioxidant effects and has recently been approved for the treatment of inflammation, pain, and spasticity associated with multiple sclerosis in patients, in a mouse model of cisplatin‐induced nephropathy. Cisplatin induced increased expression of superoxide generating enzymes RENOX and NOX1,, enhanced ROS generation, nitrotyrosine formation, apoptosis , PARP activity, and inflammation in the kidneys of mice, associated with marked histopathological damage and impaired renal function. Pretreatment of mice with cannabidiol markedly attenuated the cisplatin‐induced oxidative/nitrosative stress, inflammation and cell death in the kidney, and improved renal function. Thus, our results suggest that cannabidiol may represent a promising new protective strategy against cisplatin‐induced nephrotoxicity.