Modulation of oxidative stress in psoriasis: Pathophysiology and therapy

Psoriasis is a chronic diseases caused by interactions between immune cells and keratinocytes, which take place via different cytokines. Nevertheless current studies show that important role in regulation of inflammation in psoriasis is played by ROS, RNS, and different lipid mediators. In psoriasis increased ROS generation leads to oxidative stress and in consequence oxidative modifications of macromolecules such as proteins and lipids in both immune and skin cells. This causes the activation of transcription factors and increased apoptosis of cells. Additionally products of non-enzymatic lipid modifications like 4-HNE or isoprostanes as well as some products of enzymatic lipid metabolism (most prostaglandins) increases pro-inflammatory signaling in psoriasis. On the other hand, other group of lipid mediators-endocannabinoids and their receptors are believed to be generated more intensively as a kind of compensatory mechanism to counteract oxidative stress and inflammation. However, their action in psoriasis is insufficient to restore the physiological state. Still, due to importance of redox and lipid signaling in psoriasis different therapies which affecting them are under development. Most promising anti-oxidative drugs whose use is being considered in psoriasis are: cannabidiol, dimethyl fumarate, propylthiouracil, curcumin, luteolin.