|cannabis||liver in humans via survey (n=22366)||Inverse association of marijuana use with nonalcoholic fatty liver disease among adults in the United States.||Oct 2017|
|Positive In this nationally representative sample, active marijuana use provided a protective effect against NAFLD independent of known metabolic risk factors. The pathophysiology is unclear and warrants further investigation.|
|cannabinoids||liver via review||Endocannabinoid System in Hepatic Glucose Metabolism, Fatty Liver Disease, and Cirrhosis.||May 2019|
|The ECS system is highly upregulated during chronic liver disease and a growing number of studies suggest a mechanistic and therapeutic impact of ECS on the development of liver fibrosis, especially putting its receptors into focus.|
|cannabinoids||liver,diabetes via review||The Role of Endocannabinoids System in Fatty Liver Disease and Therapeutic Potentials||Jul 2013|
|There is accumulating evidence on the role CB1 as a key mediator of insulin resistance and liver lipogenesis in both animals and humans. On the other hand, CB2 receptors have been shown to promote inflammation with anti-fibrogenic properties. The pharmacological modulation of the EC system activity for the treatment of metabolic syndrome and NAFLD are promising yet premature.|
|Rimonabant||cholesterol,liver in humans via placebo trial (n=803)||Effect of rimonabant on the high-triglyceride/ low-HDL-cholesterol dyslipidemia, intraabdominal adiposity, and liver fat: the ADAGIO-Lipids trial.||Mar 2009|
Ingestion Method: 20mg/day|
In abdominally obese patients with atherogenic dyslipidemia, rimonabant 20 mg significantly improved multiple cardiometabolic risk markers and induced significant reductions in both intraabdominal and liver fat.
|cannabinoids||liver in vitro via experiment||Antifibrogenic role of the cannabinoid receptor CB2 in the liver.||Mar 2005|
Action Pathway: CB2|
These data constitute the first demonstration that CB2 receptors are highly up-regulated in the cirrhotic liver, predominantly in hepatic fibrogenic cells. Moreover, this study also highlights the antifibrogenic role of CB2 receptors during chronic liver injury.
|JWH-133||liver in mice via experiment||Cannabinoid-2 receptor mediates protection against hepatic ischemia/reperfusion injury||Feb 2007|
|These findings suggest that oxidative/nitrosative stress and inflammatory stimuli may trigger endocannabinoid production, and indicate that targeting CB2 cannabinoid receptors may represent a novel protective strategy against I/R injury|
|cannabinoids||liver via review||CB2 receptors as new therapeutic targets for liver diseases||Jan 2008|
|Recent data have unravelled a key role of CB2 receptors during chronic and acute liver injury, including fibrogenesis associated to chronic liver diseases, ischaemia-reperfusion-induced liver injury, and hepatic encephalopathy associated to acute liver failure. This review summarizes the latest advances on the recently identified role of CB2 receptors in the pathophysiology of liver diseases.|
|cannabinoids||liver via review||The endocannabinoid system and liver diseases.||May 2008|
|At present, the CB(1) antagonists represent the most attractive pharmaceutical tool to resolve fat accumulation in patients with non-alcoholic fatty liver disease and to treat patients with cirrhosis, as they may slow the progression of fibrosis and attenuate the cardiovascular alterations associated with the advanced stage of the disease.|
|cannabinoids||liver via review||The Role of Cannabinoids in the Setting of Cirrhosis||Jun 2018|
|The endocannabinoid system has been shown to play a role in liver disease, and cirrhosis specifically, with intriguing possible therapeutic benefits.|
|THC,JWH-015||cancer,liver in vitro||Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy||Jul 2011|
Action Pathway: CB2|
We found that delta-9-tetrahydrocannabinol (delta-9-THC, the main active component of Cannabis sativa) and JWH-015 (a cannabinoid receptor 2 (CB2) cannabinoid receptor-selective agonist) reduced the viability of the human HCC cell lines HepG2 (human hepatocellular liver carcinoma cell line) and HuH-7 (hepatocellular carcinoma cells), an effect that relied on the stimulation of CB2 receptor.