Physiological Role of Targeting of the Receptor for Advanced Glycation End Products and Its Involvement in Severe Acute Pancreatitis

Leukocyte infiltration and damage to pancreatic acinar cells serve as key indicators of severeacute pancreatitis (AP) [1]. However, the signaling pathways involved in pancreaticinflammation and tissue damage remain unclear. This study explores the impact of inhibitingthe receptor for advanced glycation end products (RAGE) signaling in AP. We examined therole of RAGE signaling by administering a RAGE inhibitor (anti-RAGE) (500 µg/kg) to C57BL/6mice prior to inducing pancreatitis with taurocholate injection into the pancreatic duct. AntiRAGE treatment led to a reduction in blood amylase levels, neutrophil infiltration in thepancreas, hemorrhage, and edema caused by taurocholate-induced pancreatitis. Additionally,anti-RAGE administration lowered MPO activity in both the pancreas and lungs.