November 12, 2014
Notes: Xu, Ping
Research Support, Non-U.S. Gov’t
Dig Dis Sci. 2013 Dec;58(12):3516-23. doi: 10.1007/s10620-013-2842-3. Epub 2013 Nov 2.
Author Address: Department of Gastroenterology, Songjiang Hospital Affiliated First People’s Hospital, Shanghai Jiao Tong University, Shanghai, 201600, China, email@example.com.
Reference Type: Journal Article
Record Number: 4825Author: Xu, P., Wang, J., Yang, Z. W., Lou, X. L. and Chen, C.
Title: Regulatory roles of the PI3K/Akt signaling pathway in rats with severe acute pancreatitis
Journal: PLoS One
Short Title: Regulatory roles of the PI3K/Akt signaling pathway in rats with severe acute pancreatitis
Alternate Journal: PloS one
ISSN: 1932-6203 (Electronic)
Accession Number: 24312352
Abstract: The phosphatidylinositol 3-kinase(PI3K)/protein kinase B (Akt) pathway plays a key role in inflammation. However, the regulatory roles of PI3K/Akt in severe acute pancreatitis (SAP) have not been elucidated. The aim of this study was to investigate the impact of wortmannin, a PI3K/Akt inhibitor, on SAP rats through exposure to sodium taurocholate (STC) after 3 h and 6 h. The SAP group was found to have a significant increase in pancreas Akt expression, along with the activation of serum amylase, TNF-alpha, IL-1beta, and IL-6, and pancreas histological aggravation. The administration of wortmannin in SAP rats reduced Akt expression, attenuated the level of serum amylase and inflammation factor, and alleviated the damage of pancreatic tissue. Furthermore, the administration of wortmannin led to an obvious reduction in NF-kappaB and p38MAPK expression in SAP rats. These findings showed that the PI3K/Akt inhibitor wortmannin decreases inflammatory cytokines in SAP rats and suggests its regulatory mechanisms may occur through the suppression on NF-kappaB and p38MAPK activity.