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. 2017 Oct 25;18(11):2239. doi: 10.3390/ijms18112239

Figure 1.

Figure 1

Proposed mechanisms of action of docosahexaenoic acid (DHA) in cerulein-induce acute pancreatitis. Cerulein induced the activation of NADPH oxidase, which produces large amounts of reactive oxygen species (ROS) in pancreatic acinar cells. ROS activate protein kinase C-δ (PKC-δ), which activates nuclear factor-κB (NF-κB). ROS also directly activate NF-κB, activator protein-1 (AP-1), janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3), and inflammatory cytokine expression in the cerulein-stimulated pancreatic acinar cells and rat models. The inflammatory events result in development of acute edematous pancreatitis. DHA induces activation of peroxisome proliferator-activated receptor-γ (PPAR-γ) and expression of the PPARγ-target gene, SOD1, and catalase. Since SOD1 and catalase scavenge ROS, DHA inhibits the ROS-mediated activation of inflammatory signaling (PKC-δ, NF-κB, AP-1, JAK2/STAT3) and inflammatory cytokine expression in cerulein-stimulated pancreatic acinar cells and animal models. Antioxidant and anti-inflammatory effects of DHA may be responsible for preventing the development of acute pancreatitis. The bars represent inhibition, while the arrows represent stimulation.