ATRIAL NATRIURETIC FACTOR (ANF) ALLEVI ATES ENDOPLASMIC RETICULUM STRESS IN RAT ACUTE PANCREATITIS

COURREGES AP; NAJENSON AC; VATTA MS; BIANCIOTTI LG

Mar del Plata

Congreso; LXI ANNUAL MEETING ARGENTINE SOCIETY FOR CLINICAL INVESTIGATION (SAIC) LXIV ANNUAL MEETING ARGENTINE SOCIETY OF IMMUNOLOGY (SAI) XLVIII ANNUAL MEETING ARGENTINE SOCIETY OF EXPERIMENTAL PHARMACOLOGY (SAFE) VII ANNUAL MEETING ARGENTINE SOCIETY OF NA; 2016

SAIC-SAI-SAFE-NANOMEDAR-AACYTAL

The endoplasmic-reticulum (ER) stress response constitutesa cellular process that is triggered by a variety of conditions thatdisturb proteins folding in the ER. Eukaryotic cells have developedan evolutionarily conserved adaptive mechanism, the unfoldedprotein response (UPR), which aims to clear unfolded proteinsand restore ER homeostasis. Recent studies support that the ERstress is one of the earliest events triggering acute pancreatitis(AP). Based on previous findings from our laboratory showing thatANF significantly attenuates the severity of AP by reducing tryp-sinogen activation and the inflammatory response, we sought toestablish whether ANF affected ER stress in a validated AP animalmodel. AP was induced in Sprague Dawley strain rats (200-220g) by four repetitive cerulein injections (40 μg/kg). Thirty minutesbefore the first cerulein injection animals were infused with eithersaline (control) or ANF (1 μg/kg/h) for 60 min. Following euthanasiapancreatic samples were harvested for western blot analysis andtransmission electronic microscopy (TEM) studies. ChaperoneBiP, the primary controller of UPR, was overexpressed in ceruleininduced AP (p < 0,001) but pretreatment with ANF prevented it (p