Figure 2.

Cyclooxygenases 1 and 2 (COX-1 and COX-2), which are key enzymes in the conversion of arachidonic acid into bioactive prostanoids play a central role in the inflammatory cascade. Prostaglandin families (postaglandin J2) are endogenous toxic products of cyclooxygenases, and because their levels are significantly increased upon brain injury, they are actively involved in neuronal dysfunction induced by pro-inflammatory stimuli. The line of evidence indicates an important interplay between the cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2) and endocannabinoids (ECB) are key inflammatory and redox-dependent processes. The endocannobinoid system (ECS) may also control oxidative stress by directly or indirectly modulating CB1 and CB2 signaling or CB receptor-independent processes via COX-2-dependent eicosanoid pathway. Modulation of cellular redox homeostasis is induced by the ECS. The reactive oxygen species (ROS) act as second messengers and exert oxidative activity to influence immune, inflammatory, and other signaling processes.