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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

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

Hao Pan, Partha Mukhopadhyay, Mohanraj Rajesh, Vivek Patel, Bani Mukhopadhyay, Bin Gao, György Haskó and Pál Pacher
Journal of Pharmacology and Experimental Therapeutics March 2009, 328 (3) 708-714; DOI: https://doi.org/10.1124/jpet.108.147181
Hao Pan
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Partha Mukhopadhyay
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Mohanraj Rajesh
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Vivek Patel
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Bani Mukhopadhyay
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Bin Gao
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György Haskó
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Pál Pacher
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Abstract

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-α and interleukin-1β) 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.

Footnotes

  • This study was supported by the Intramural Research Program of National Institutes of Health National Institute on Alcohol Abuse and Alcoholism.

  • H.P. and P.M. contributed equally to this work.

  • doi:10.1124/jpet.108.147181.

  • ABBREVIATIONS: PARP, poly(ADP-ribose) polymerase; TNF, tumor necrosis factor; IL, interleukin; CB, cannabinoid; CBD, cannabidiol; BUN, blood urea nitrogen; iNOS, inducible nitric-oxide synthase; PAS, periodic acid-Schiff; ROS, reactive oxygen species; MDA, malondialdehyde; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling staining; ELISA, enzyme-linked immunosorbent assay; PCR, polymerase chain reaction; CP, cisplatin; NT, 3-nitrotyrosine.

    • Received October 8, 2008.
    • Accepted December 11, 2008.
  • U.S. Government work not protected by U.S. copyright
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Journal of Pharmacology and Experimental Therapeutics: 384 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 384, Issue 2
1 Feb 2023
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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

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

Hao Pan, Partha Mukhopadhyay, Mohanraj Rajesh, Vivek Patel, Bani Mukhopadhyay, Bin Gao, György Haskó and Pál Pacher
Journal of Pharmacology and Experimental Therapeutics March 1, 2009, 328 (3) 708-714; DOI: https://doi.org/10.1124/jpet.108.147181

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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

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

Hao Pan, Partha Mukhopadhyay, Mohanraj Rajesh, Vivek Patel, Bani Mukhopadhyay, Bin Gao, György Haskó and Pál Pacher
Journal of Pharmacology and Experimental Therapeutics March 1, 2009, 328 (3) 708-714; DOI: https://doi.org/10.1124/jpet.108.147181
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