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Research Library

A-Z Conditions  Participate in ORR

Cannabidiol Attenuates Cisplatin-Induced Nephrotoxicity by Decreasing Oxidative/Nitrosative Stress, Inflammation, and Cell Death

  • Journal : Journal of Pharmacology and Experimental Therapeutics
  • Publication Year : 2008
  • Authors : Hao Pan, Partha Mukhopadhyay, Mohanraj Rajesh, Vivek Patel, Bani Mukhopadhyay, Bin Gao, György Haskó, Pál Pacher

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 (NOX4) and NOX1, enhanced reactive oxygen
species generation, inducible nitric-oxide synthase expression,
nitrotyrosine formation, apoptosis (caspase-3/7 activity, DNA
fragmentation, and terminal deoxynucleotidyl transferase dUTP
nick-end labeling staining), poly(ADP-ribose) polymerase activity,
and inflammation (tumor necrosis factor- and interleukin-1) in
the kidneys of mice, associated with marked histopathological
damage and impaired renal function (elevated serum blood urea
nitrogen and creatinine levels) 72 h after the administration of the
drug. Treatment of mice with cannabidiol markedly attenuated
the cisplatin-induced oxidative/nitrosative stress, inflammation,
and cell death in the kidney, and it improved renal function.
Thus, our results suggest that cannabidiol may represent a
promising new protective strategy against cisplatin-induced
nephrotoxicity.

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