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BioMed Research International
Volume 2016 (2016), Article ID 6089430, 10 pages
Research Article

Aspirin Protects against Acinar Cells Necrosis in Severe Acute Pancreatitis in Mice

1Surgical Intensive Care Unit (SICU), Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, No. 305 Zhongshan East Road, Nanjing, Jiangsu Province 210002, China
2Department of Gastroenterology, Affiliated Hospital of Yangzhou University, Yangzhou, China
3Key Laboratory of Molecular Cardiovascular Science Ministry of Education, Institute of Cardiovascular Science, Peking University, Beijing, China
4Department of Emergency, Zhejiang Provincial People’s Hospital, Zhejiang, China

Received 11 July 2016; Revised 7 November 2016; Accepted 23 November 2016

Academic Editor: Andrea Mencarelli

Copyright © 2016 Guotao Lu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aspirin has a clear anti-inflammatory effect and is used as an anti-inflammatory agent for both acute and long-term inflammation. Previous study has indicated that aspirin alleviated acute pancreatitis induced by caerulein in rat. However, the role of aspirin on severe acute pancreatitis (SAP) and the necrosis of pancreatic acinar cell are not yet clear. The aim of this study was to determine the effects of aspirin treatment on a SAP model induced by caerulein combined with Lipopolysaccharide. We found that aspirin reduced serum amylase and lipase levels, decreased the MPO activity, and alleviated the histopathological manifestations of pancreas and pancreatitis-associated lung injury. Proinflammatory cytokines were decreased and the expression of NF-κB p65 in acinar cell nuclei was suppressed after aspirin treatment. Furthermore, aspirin induced the apoptosis of acinar cells by TUNEL assay, and the expression of Bax and caspase 3 was increased and the expression of Bcl-2 was decreased. Intriguingly, the downregulation of critical necrosis associated proteins RIP1, RIP3, and p-MLKL was observed; what is more, we additionally found that aspirin reduced the COX level of pancreatic tissue. In conclusion, our data showed that aspirin could protect pancreatic acinar cell against necrosis and reduce the severity of SAP. Clinically, aspirin may potentially be a therapeutic intervention for SAP.