Interventions of natural and synthetic agents in inflammatory bowel disease, modulation of nitric oxide pathways

Figure 1 Main cellular mechanism of interventions in inflammatory bowel disease. COX-2: Cyclooxygenase-2; iNOS: Inducible nitric oxide synthase; TNF-α: Tumor necrosis factor alpha; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; IκB: Inhibitor of kappa B; IKκ complex: Inhibitor of kappa kinase complex; MyD88: Myeloid differentiation primary response 88; P38MAPK: P38Mitogen-activated protein kinase; GSH: Glutathione; P13k: Phosphatidylinositol 13-kinase; STAT: Signal transducer and activator of transcription proteins; IL-6: Interleukin-6; IL-1: Interleukin-1; PPARγ: Peroxisome proliferator-activated receptor gamma; TLR: Toll-like receptor; MCP-1: Monocyte chemoattractan-t protein-1; AP-1: Activator protein 1; IRAK: Interleukin-1 receptor-associated kinase; NAC: N-acetyl cysteine; NO: Nitric oxide; SOD: Superoxide dismutase; CAT: Catalase; TGFβR: Transforming growth factor beta receptor I.

Figure 2 Inhibition of nitric oxide synthase suppresses inflammatory bowel disease. IBD: Inflammatory bowel disease; NOS: Nitric oxide synthase; NO: Nitric oxide.