Cannabis sativa L. and Nonpsychoactive Cannabinoids: Their Chemistry and Role against Oxidative Stress, Inflammation, and Cancer

Figure 2

General representation of the signaling pathways involved in CBD anti-inflammatory effects. Cannabinoids reduce peripheral inflammation by acting at TRPV1, CB₂, and GPR55 receptors; these interactions lead to downregulation of enzymes involved in the production of prostaglandins, reactive oxygen species, and cytokines. MAPK inhibition and NF-kB downregulation, together with PPARγ-mediated reduction of lipid peroxidation, are also involved in the anti-inflammatory effects of cannabinoids in the CNS. Abbreviations: CBD, cannabidiol; CNS, central nervous system, CB₂, cannabinoid receptor 2; TRPV1, receptor potential channel subfamily V member 1; GPR55, orphan G-protein coupled receptor 55; Akt, protein kinase B; ERK, extracellular signal-regulated kinases; NF-kB nuclear factor kappa-light-chain-enhancer of activated B cells; iNOS, inducible nitric oxide synthase; COX2, cyclooxygenase 2; TNF-α, tumor necrosis factor alpha; PPARγ, peroxisome proliferator-activated receptor gamma.