Chrm3 protects against acinar cell necrosis by stabilizing caspase‐8 expression in severe acute pancreatitis mice model

2019 ◽  
Vol 121 (3) ◽  
pp. 2618-2631 ◽  
Author(s):  
Ning Huang ◽  
Ghulam Murtaza ◽  
Lujing Wang ◽  
Jing Luan ◽  
Xinlei Wang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Acinar Cell ◽  
Caspase 8 ◽  
Cell Necrosis ◽  
Mice Model ◽  
Acinar Cell Necrosis

NQDI-1 protects against acinar cell necrosis in three experimental mouse models of acute pancreatitis

2019 ◽  
Vol 520 (1) ◽  
pp. 211-217 ◽  
Author(s):  
Xiaochun Xie ◽  
Chenchen Yuan ◽  
Ling Yin ◽  
Qingtian Zhu ◽  
Nan Ma ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Mouse Models ◽  
Acinar Cell ◽  
Cell Necrosis ◽  
Experimental Mouse ◽  
Acinar Cell Necrosis

scholarly journals Anti-inflammatory and Anti-necrotic Effect of Lectins from Canavalia ensiformis and Canavalia brasiliensis in Experimental Acute Pancreatitis

2021 ◽  
Author(s):  
Samara Rodrigues Bonfim Damasceno Oliveira ◽  
Álvaro Xavier Franco ◽  
Marielle Pires Quaresma ◽  
Cecília Mendes Morais de Carvalho ◽  
Fabrícia da Cunha Jácome Marques ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Cell Death ◽  
Acinar Cell ◽  
Acinar Cells ◽  
Pancreatic Acinar Cell ◽  
Cell Necrosis ◽  
Experimental Acute Pancreatitis ◽  
Canavalia Ensiformis ◽  
Acinar Cell Necrosis ◽  
Canavalia Brasiliensis

Abstract Lectins isolated from Canavalia ensiformis (ConA) and Canavalia brasiliensis (ConBr) are promising molecules to modulate cell death. Acute pancreatitis, characterized by acinar cell necrosis and inflammation, presents significant morbidity and mortality. This study has investigated the effects of ConA and ConBr on experimental acute pancreatitis and pancreatic acinar cell death induced by bile acid. Pancreatitis was induced by retrograde pancreatic ductal injection of 3% sodium taurocholate (Na-TC) in male Swiss mice. ConA or ConBr (0.1, 1 or 10 mg/kg) were intravenously applied to mice 1 h and 12 h after induction. After 24 hours, the severity of pancreatitis was evaluated by serum amylase and lipase, histopathological changes and myeloperoxidase assay. Pancreatic acinar cells were incubated with ConA (200 µg/ml) or ConBr (200 µg/ml) and taurolithocholic acid 3-sulfate (TLCS; 500 µM). Necrosis and changes in mitochondrial membrane potential (ΔѰm) were detected by fluorescence confocal microscopy. Treatment (post-insult) with ConA and ConBr decreased pancreatic damage caused by retrograde injection of Na-TC in mice, reducing pancreatic neutrophil infiltration, edema and necrosis. In addition, ConA and ConBr decreased pancreatic acinar cell necrosis and depolarization of ΔѰm caused by TLCS. The inhibition of necrosis was prevented by the lectin domain blockade; molecular docking analysis showed strong interaction of ConA and ConBr crystal structures with mannose residues. In conclusion, ConA and ConBr markedly inhibited in vitro and in vivo damage, effects partly dependent on the interaction with mannose residues on acinar cells. These data support the potential application of these proteins for treatment of acute pancreatitis.

373 Mechanisms Mediating Acinar Cell Necrosis and Autophagy in Experimental Acute Pancreatitis: the Role of PI3K Gamma

2009 ◽  
Vol 136 (5) ◽  
pp. A-61
Author(s):  
Wenzhuo Jia ◽  
Lars Fischer ◽  
Jae Hyuk Do ◽  
Sheyla Perez ◽  
Anna S. Gukovskaya ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Acinar Cell ◽  
Cell Necrosis ◽  
Experimental Acute Pancreatitis ◽  
Pi3k Gamma ◽  
Acinar Cell Necrosis

scholarly journals Diabetic Bone Marrow Cell Injection Accelerated Acute Pancreatitis Progression

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Xiao-Min Luo ◽  
Cen Yan ◽  
Yue-Jie Zhang ◽  
Ling-Jia Meng ◽  
Guo-Tao Lu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Pancreatitis ◽  
Acinar Cell ◽  
Cell Injury ◽  
Bone Marrow Cells ◽  
Marrow Cell ◽  
Cell Necrosis ◽  
Serum Lipase ◽  
Cell Injection ◽  
Acinar Cell Necrosis

Acute pancreatitis (AP) is one of the leading causes of hospital admission, 20% of which could progress to the severe type with extensive acinar cell necrosis. Clinical studies have reported that diabetes is an independent risk factor of the incidence of AP and is associated with higher severity than nondiabetic subjects. However, how diabetes participates in AP progression is not well defined. To investigate this question, wild-type (wt) and diabetic db/db mice at the age of 16 weeks were used in the study. AP was induced in wt recipients by 10 injections of 50 μg/kg caerulein with a 1 h interval. One hour after the last caerulein injection, bone marrow cells (BMC) isolated from wt and db/db mice were injected intraperitoneally into the recipients ( 1 × 10 7 cells/recipient). The recipients with no BMC injection served as controls. Thirteen hours after BMC injection, serum lipase activity was 1.8- and 1.3-folds higher in mice that received db/db BMC, compared with those with no injection and wt BMC injection, respectively ( p ≤ 0.02 for both). By H&E staining, the overall severity score was 14.7 for no cell injection and 16.6 for wt BMC injection and increased to 22.6 for db/db BMC injection ( p ≤ 0.002 for both). In particular, mice with db/db BMC injection developed more acinar cell necrosis and vacuolization than the other groups ( p ≤ 0.03 for both). When sections were stained with an antibody against myeloperoxidase (MPO), the density of MPO+ cells in pancreatitis was 1.9- and 1.6-folds higher than wt BMC and no BMC injection groups, separately ( p ≤ 0.02 for both). Quantified by ELISA, db/db BMC produced more IL-6, GM-CSF, and IL-10 compared with wt BMC ( p ≤ 0.04 for all). In conclusion, BMC of db/db mice produced more inflammatory cytokines. In response to acinar cell injury, diabetic BMC aggravated the inflammation cascade and acinar cell injury, leading to the progression of acute pancreatitis.

scholarly journals TRPM2‐mediated extracellular Ca 2+ entry promotes acinar cell necrosis in biliary acute pancreatitis

2020 ◽  
Vol 598 (6) ◽  
pp. 1253-1270 ◽  
Author(s):  
Júlia Fanczal ◽  
Petra Pallagi ◽  
Marietta Görög ◽  
Gyula Diszházi ◽  
János Almássy ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Acinar Cell ◽  
Cell Necrosis ◽  
Biliary Acute Pancreatitis ◽  
Acinar Cell Necrosis

scholarly journals Chemokine CXCL16 mediates acinar cell necrosis in cerulein induced acute pancreatitis in mice

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Yojiro Sakuma ◽  
Yuzo Kodama ◽  
Takaaki Eguchi ◽  
Norimitsu Uza ◽  
Yoshihisa Tsuji ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Acinar Cell ◽  
Cell Necrosis ◽  
Acinar Cell Necrosis

Ligation-Induced Acute Pancreatitis in Opossums: Acinar Cell Necrosis in the Absence of Colocalization

1995 ◽  
Vol 58 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Isaac Samuel ◽  
Daniel P. Wilcockson ◽  
Joseph P. Regan ◽  
Raymond J. Joehl
Keyword(s):  
Acute Pancreatitis ◽  
Acinar Cell ◽  
Cell Necrosis ◽  
Acinar Cell Necrosis
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