Cannabinoids are chemical compounds that are located in the marijuana plant (cannabis sativa). Cannabidiol (CBD) is one of these compounds and studies have shown it has anti inflammatory effects when induced on animal cells. People have smoked cannabis for thousands of years and it has said have an anti inflammatory role in the body. Tetrahydrocannabinol (THC) is another one of these chemicals and it is said it has psychoactive effects. Cannabinoid receptors (CB1 and CB2) are found in the endocannabinoid system and allow cannabinoids to thrive in the body. While cannabinoids have displayed to relieve liver fibrosis, their impacts in chronic pancreatitis and on pancreatic stellate cells (PSC) are not yet known. In this study, levels of endocannabinoids and their receptors were measured as well as the potential role of cannabinoid triggering by synthetic cannabinoid derivatives and their respective antagonists in human chronic pancreatitis tissues.
Besides the well-known central-nervous therapeutic effects of cannabinoids, the endocannabinoid system (ECS) and its changes in pathological states have recently attracted interest from the scientific community. Particularly, cannabinoids’ immune-modulatory role and their influence in treating inflammatory diseases. Besides these well-studied effects, endocannabinoids have recently been shown to influence liver fibrogenesis through various mechanisms. In a previous study, it was shown that the endocannabinoid anandamide induces death in malignant cells. In contrast to these results,it was found in experimentally induced liver cirrhosis that an activation of the CB2 receptor on malignant cells leads to apoptosis and attenuated liver fibrosis progression. Altogether, these results point towards a potential role of cannabinoids as drugs to alleviate or even revert liver fibrogenesis. However, the exact mechanism of how either triggering the cannabinoid receptor may be useful in attenuating chronic liver cirrhosis remains to be determined.
Modulation of the endocannabinoid system via cannabinoid inducing, might actually be a reasonable option to treat inflammation and fibrosis in chronic pancreatitis. This means that cannabinoids could be possibly be used as effective treatments for acute inflammation as it has minimal side effects in the central nervous system. In conclusion, this paper shows that the endocannabinoid system is downregulated in chronic pancreatitis and that its augmentation via exogenously administered cannabinoids specifically reduces activation of pancreatic stellate cells. These experiments lay a basis for testing the value of synthetic cannabinoids in the treatment of chronic pancreatitis.