Phytocannabinoids in the Pharmacotherapy of Psoriasis

Abstract

Phytocannabinoids are naturally occurring compounds, the main source of which is Cannabis sativa L. Through direct action or interaction with G protein-coupled receptors, they affect ROS and pro-inflammatory cytokines levels and modify the effectiveness of transcription factor responsible for the biosynthesis of antioxidants which lead to oxidative stress and its consequences. Due to the modification of the redox balance and inflammation, phytocannabinoids are used in the treatment of various diseases, including autoimmune dermatoses, such as atopic dermatitis and psoriasis. Psoriasis is one of the most common dermatoses, and one of unknown etiology. A disturbed redox balance with a shift towards the oxidation leads to oxidative stress, resulting in oxidative modifications, mainly of lipids and proteins, and prolonged activation of immune cells and increased generation of pro-inflammatory cytokines, resulting in chronic inflammation. Given the biological activity of phytocannabinoids, they have become the focus of research as components of pharmacotherapy for psoriasis. Beneficial effects were shown by various representatives of phytocannabinoids, but the effect of cannabidiol (CBD) on skin cells (in vitro and ex vivo) and on blood cells from patients with psoriasis vulgaris and psoriatic arthritis has been most often evaluated in recent years.

Keywords: CBD; blood cells; inflammation; oxidative stress; phytocannabinoids; psoriasis; skin cells.

Figure 1

Division of phytocannabinoids by chemical structure along with chemical formulas of the main representatives of each class.

Figure 2

The effect of cannabidiol (CBD) on redox imbalance, inflammation and their metabolic consequences in the keratinocytes of patients with Psoriasis. Abbreviations: 4-HNE—4-hydroxynonenal; 8-isoPs—8-isoprostanes; Bach1—protein; CB1—cannabinoid receptor 1; CB2—cannabinoid receptor 2; COX—cyclooxygenase; FAAH—fatty acid amide hydrolase; Keap1—kelch-like ECH-associated protein 1; LOX—lipoxygenase; MAGL—monoacylglycerol lipase; MDA—malondialdehyde; NeuroPs—neuroprostanes; NFκB—nuclear factor kappa-B; Nrf2—nuclear factor erythroid 2; p65—nuclear factor NF-kappa-B p65 subunit; PLA2—phospholipase A2; PPARs—peroxisome; proliferator-activated receptors; PUFAs—polyunsaturated fatty acids; TNFα—tumor necrosis factor alpha.