Li J.,University of Sichuan |
Li J.,Key Laboratory of Biotherapy of Human Diseases |
Zhou C.,University of Sichuan |
Wang R.,Key Laboratory of Biotherapy of Human Diseases |
And 4 more authors.
Alcoholism: Clinical and Experimental Research | Year: 2010
Background: Long-term alcohol consumption alone did not cause chronic pancreatitis (CP) but impaired exocrine pancreatic function. This study is to explore the reversibility of exocrine pancreatic insufficiency in the abstinent rats and its mechanism.Methods: Forty-eight healthy male Wistar rats were divided randomly into 4 groups: 6-month control, 6-month ethanol, 9-month control, and 9-month ethanol + withdrawal. Morphological changes of pancreatic acinar cells were observed. Pancreatic amylase and lipase were measured using an automatic biochemical analyzer. Free fatty acid (FFA) in rat intestinal chyme was measured. Cholecystokinin (CCK) levels were determined by radioimmunoassay. The expression of CCK-A receptors was quantitatively analyzed by Western blot.Results: Alcohol-induced ultramicrostructure changes of pancreatic acinar cells, including lipid droplets, myelinoid inclusion bodies, dilated rough endoplasmic reticulums, and diminished zymogen granules, were not attenuated after alcohol abstinence. The outputs of amylase and lipase, FFA content in intestinal chyme, and the intestinal and the pancreatic CCK levels in rats were reduced after chronic alcohol intake and were still lower than the control after cessation of alcohol use. Chronic ethanol intake or abstinence did not induce any change in the expression of CCK-A receptors.Conclusions: Exocrine pancreatic insufficiency was irreversible in alcoholic rats without CP after alcohol withdrawal. It may be attributed to reduced pancreatic CCK, long-standing fatty infiltration, ultramicrostructure injuries in pancreatic acinar cells, and aging. © 2010 by the Research Society on Alcoholism.
Chen P.,University of Sichuan |
Hu B.,University of Sichuan |
Tan Q.,Key Laboratory of Biotherapy of Human Diseases |
Liu L.,University of Sichuan |
And 5 more authors.
Neurogastroenterology and Motility | Year: 2010
Background Intestinal ischemia-reperfusion (IIR) is implicated in the pathogenesis of severe acute pancreatitis (SAP). This study investigates the impact of neurocrine somatostatin (SST) on the contraction of sphincter of Oddi (SO) during IIR. Methods Intestinal ischemia-reperfusion model in macaques was induced by occluding the superior mesenteric artery. Pancreatitis was confirmed by pancreatic histology and serum levels of amylase and lipase. SST and its receptors (SSTRs) in SO were visualized by immunohistochemistry. Effects of SST on the contraction of the isolated SO were recorded in vitro. Key Results Inflammatory scores of the pancreas and serum levels of amylase or lipase in the macaques that underwent IIR were significantly higher than those in the control group. The frequency and amplitude of phasic contraction of the circular muscle in SO was increased by SST in a concentration-dependent manner. Compared with the control group, SST innervation or SSTR2 expression in SO of macaques treated with IIR was increased 5.2 fold or 5.6 fold respectively. Prophylactic infusion of SST before IIR significantly reduced SST immunoreactive fibers in SO as compared to those in the IIR group and remarkably alleviated the pathophysiologic changes due to IIR. Conclusions & Inferences Increased SST innervation in SO during the early phase of IIR associated with the contraction of circular muscle of SO, which might be one of the promoting factors associated with the development of SAP. Prevention of IIR or intervention of SO contraction after occurrence of acute pancreatitis might be beneficial for preventing SAP. © 2010 Blackwell Publishing Ltd.
Li J.,University of Sichuan |
Yang W.-J.,Key Laboratory of Biotherapy of Human Diseases |
Huang L.-M.,University of Sichuan |
Tang C.-W.,University of Sichuan
World Journal of Gastroenterology | Year: 2014
It is currently difficult for conventional treatments of acute pancreatitis (AP), which primarily consist of antiinflammatory therapies, to prevent the progression of AP or to improve its outcome. This may be because the occurrence and progression of AP, which involves various inflammatory cells and cytokines, includes a series of complex immune events. Considering the complex immune system alterations during the course of AP, it is necessary to monitor the indicators related to immune cells and inflammatory mediators and to develop more individualized interventions for AP patients using immunomodulatory therapy. This review discusses the recent advances in immunomodulatory therapies. It has been suggested that overactive inflammatory responses should be inhibited and excessive immunosuppression should be avoided in the early stages of AP. The optimal duration of anti-inflammatory therapy may be shorter than previously expected (< 24 h), and appropriate immunostimulatory therapies should be administered during the period from the 3rd d to the 14th d in the course of AP. A combination therapy of anti-inflammatory and immune-stimulating drugs would hopefully constitute an alternative to anti-inflammatory drug monotherapy. Additionally, the detection of the genotypes of critical inflammatory mediators may be useful for screening populations of AP patients at high risk of severe infections to enable the administration of early interventions to improve their prognosis. © 2014 Baishideng Publishing Group Inc. All rights reserved.