Co-operative effects of angiotensin II and caerulein in NFκB activation in pancreatic acinar cells in vitro.

摘要: Abstract Angiotensin II is a vasoactive peptide that controls blood pressure and homeostasis. Emerging evidence shows locally generated angiotensin plays crucial role in normal physiology, as well pathophysiological conditions such pancreatitis. We recently reported activates pancreatic NFκB obstructive However, the specific cell type responsible for this activation remains unclear. In study, we investigated whether acinar cells respond to II. These are most abundant vulnerable Pancreatic AR42J were used an vitro model of inflammation. Our results demonstrated treatment with caerulein, cholecystokinin receptor agonist, induced hypersecretion activation, by elevated amylase secretion degradation inhibitor (IκBβ). II, either alone or combination augmented IκBβ degradation. Pre-treatment losartan, antagonist I (AT 1 ) receptor, abolished caerulein dose-dependent manner. Treatment PD123319, blocker 2 enhanced caerulein. Preliminary data further could extend caerulein-induced ERK1/2 cells. indicated inflammation triggered hyperstimulation via AT receptor. contrast, stimulation protects against activation. The differential roles receptors might be useful developing potential therapies