| 1 | Role of macrophages in the progression of acute pancreatitis显示文摘In addition to pancreatic cells,other inflammatory cell populations contribute to the generation of inflammatory mediators during acute pancreatitis.In particular,macrophages could be activated by mediators released during pancreatitis by a damaged pancreas.It has been reported that peritoneal macrophages,alveolar macrophages and Kupffer cells become activated in different stages of severe acute pancreatitis.However,macrophages display remarkable plasticity and can change their physiology in response to environmental cues.Depending on their microenvironmental stimulation,macrophages could follow different activation pathways resulting in marked phenotypic heterogeneity.This ability has made these cells interesting therapeutical targets and several approaches have been assayed to modulate the progression of inflammatory response secondary to acute pancreatitis.However,despite the recent advances in the modulation of macrophage function in vivo,the therapeutical applications of these strategies require a better understanding of the regulation of gene expression in these cells. | Sabrina Gea-Sorlí Daniel Closa | 2010 | World Journal of Gastrointestinal Pharmacology and Therapeutics2010，1，5： | 16 |
| 2 | Protection effect of triptoKde to Kver injury in rats with severe acute pancreatitis显示文摘BACKGROUND: The high mortality of patients with severe acute pancreatitis (SAP) is due to multiorgan dysfunction. The mechanisms of SAP are still obscure. The aim of this study was to investigate the role of nuclear factor-kappa B (NF-κB) activation in rats with SAP associated with liver injury and the protection effect of triptolide against liver injury in rats with SAP. METHODS: Ninety Wistar rats were randomly divided into three groups (n =30 each group) : severe acute pancreatitis (group P) , treatment with triptolide ( group T), and sham operation (group S). SAP models were induced by retrograde injection of 5% sodium taurocholate to the pancreatic duct. After the model was successfully established, no treatment was given to group P. In group T, triptolide (0. 05 mg/ml) was injected intraperitoneally (0.2 mg/kg). In group S, the abdominal walls of rats were opened, sutured , but not treated. The rats -were sacrificed after operation at 2, 6, and 12 hours, respectively. The serum levels of amylase (AMY) , alanine aminotransferase (ALT), tumor necrosis factor-alpha ( TNF-α) and interleukin-6 (IL-6 ) were determined at three time points (10 rats for each time point). Liver tissues were obtained to detect the activity of NF-κB and to observe their pathological changes with light and electron microscopes. RESULTS: The serum levels of AMY and ALT were higher in groups P and T than in group S. The serum AMY levels were significantly lower in group T than in group P at 12 hours after operation. The serum ALT levels were significantly lower in group T than in group P at 6, 12 hours after operation. At the three time points, the levels of TNF-α and IL-6 in groups P and T increased more significantly than in group S. In group T they were decreased more significantly than in group P at the three time points. In groups P and T, NF-κB activity in liver tissue increased more significantly than in group S at the three time points. The activity of NF-κB was higher in group P than in groups S and T at the three time points. Liver pathological damages were milder in group T than in group P under light and electron microscopes. CONCLUSIONS: NF-κB plays an important role in the pathogenesis of liver injury in rats with SAP. Triptolide can reduce pathological damage to the liver. Its mechanism is to inhibit the activity of NF-κB and to decrease the release of inflammatory mediators. | Yong-Fu Zhao, Wen-Long Zhai, Shui-Jun Zhang and Xiao-Ping Chen Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030 , Chinaand Department of General Surgery , First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052 , China | 2005 | Hepatobiliary & Pancreatic Diseases International2005，4，4： | 14 |
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