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Publication Name
World Journal of Gastrointestinal Pathophysiology
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2150-5330
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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©2014 Baishideng Publishing Group Inc.
World J Gastrointest Pathophysiol. Aug 15, 2014; 5(3): 169-177
Published online Aug 15, 2014. doi: 10.4291/wjgp.v5.i3.169
Figure 1
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Figure 1 Potential mechanism of nicotinamide adenine dinucleotide phosphate oxidase activation via cholecystokinin receptor. Cerulein and cholecystokinin (CCK) receptor binding triggers transient Ca2+ release from the endoplasmic reticulum to activate nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which is mediated by PLC and IP3. Reactive oxygen species (ROS) generated by NADPH oxidase activate IκB kinase to phosphorylate IκB in the cytosol. Phosphorylated IκB is ubiquitinated and degraded in a proteasome-dependent manner. NF-κB translocates to the nucleus and regulates expression of cytokines to participate in the pathogenesis of pancreatitis.
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