title: Downregulation of GRP78 and XIAP is correlated with apoptosis during             cerulein-induced acute pancreatitis in rats via regulation of caspase activation.
abstract: Our aim in the present study was to investigate the potential roles of the             78-kDa glucose-regulated protein (GRP78) and the X-linked inhibitor of apoptosis             protein (XIAP) in the regulation of apoptosis during cerulein-induced acute pancreatitis             (CAP). A rat CAP model was induced by injection of cerulein (50 µg/kg), and the             severity of CAP was estimated by measuring serum amylase and lipase, pancreatic             edema and histological changes. Pancreatic acinar cell apoptosis was determined             by terminal-deoxynucleotidyl-transferase-mediated dUTP nick-end labeling (TUNEL)             assay, and the expression of GRP78, XIAP and the apoptotic genes caspase-3, -7             and -9 were determined by real‑time quantitative PCR and western blotting. After             induction with cerulein, increased serum amylase and lipase, pancreatic edema,             inflammation and apoptosis were observed in CAP rats. Furthermore, the mRNA and             protein levels of GRP78 and XIAP were significantly downregulated in CAP rats,             while the mRNA levels of caspase-3, -7 and -9, as well as the cell apoptotic index             were markedly increased when compared with control rats (P<0.05). The expression             of GRP78 and XIAP was negatively correlated with caspase expression in CAP (P<0.05).             This study suggests that the downregulation of GRP78 and XIAP were correlated             with apoptosis in pancreatic acinar cells, and that this may occur through the             regulation of caspase activation during CAP.
authors.affiliation: Department of Gastroenterological Surgery, West China Hospital, Sichuan University, Sichuan, PR China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Liu
authors.forename: Zong-Guang
authors.initials: ZG
authors.lastname: Zhou
authors.forename: Bing
authors.initials: B
authors.lastname: Zhou
authors.forename: Rong
authors.initials: R
authors.lastname: Wang
authors.forename: Hui
authors.initials: H
authors.lastname: Yan
authors.forename: Yuan
authors.initials: Y
authors.lastname: Li
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D053179:Caspase 7 / Q000235:genetics / Q000378:metabolism; D053453:Caspase 9 / Q000235:genetics / Q000378:metabolism; D002108:Ceruletide / Q000633:toxicity*; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects; D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D008049:Lipase / Q000097:blood; D008297:Male; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D051636:X-Linked Inhibitor of Apoptosis Protein / Q000235:genetics / Q000378:metabolism*
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; D012333:RNA, Messenger; D051636:X-Linked Inhibitor of Apoptosis Protein; D002108:Ceruletide; D008049:Lipase; D000681:Amylases; D053148:Caspase 3; D053179:Caspase 7; D053453:Caspase 9