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Cannabidiol protects against hepatic ischemia/reperfusion injury by attenuating oxidative stress, inflammatory response, and cell death
Author(s) -
Batkai Sandor,
Mukhopadhyay Partha,
Horvath Bela,
Rajesh Mohanraj,
Hasko George,
Wink David A.,
Mechoulam Raphael
Publication year - 2011
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.25.1_supplement.639.12
Ischemia‐reperfusion (I/R) is a pivotal mechanism of liver damage following liver transplantation or hepatic surgery. Cannabidiol (CBD) is the most abundant non‐psychotropic constituent of Cannabis sativa (marijuana) plant. CBD has been reported to exert protective effects in multiple disease models and may alleviate pain and spasticity associated with multiple sclerosis in humans. In this study we investigated the effects of CBD in an in vivo mouse model of hepatic I/R injury. CBD, given prior to the induction of I/R, significantly attenuated the extent of liver damage (measured by serum alanine aminotransferase and aspartate aminotransferase levels), decreased tissue 4‐hydroxy‐2‐nonenal (HNE), nitrotyrosine (NT), tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1alpha and 2 (MIP‐1α/CCL3, MIP‐2/CXCL2), inter‐cellular adhesion molecule 1 (ICAM‐1/CD54) mRNA levels, tissue neutrophil infiltration, DNA fragmentation, PARP activity and TUNEL. The protective effect of CBD against liver damage was also preserved when given right after the ischemic episode up to 90 minutes of reperfusion, likewise in cannabinoid receptor 2 (CB 2 ) knockout mice. These findings suggest that CBD may represent a novel, protective strategy against I/R injury by attenuating oxidative/nitrative stress, acute and chronic inflammatory response, and cell death, independent from CB 2 receptors.