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Protective And Therapeutic Effects Of Emodin On Lung Injury In Rats With Severe Acute Pancreatitis

Posted on:2008-06-27Degree:MasterType:Thesis
Country:ChinaCandidate:X X WangFull Text:PDF
GTID:2144360215463627Subject:General surgery
Abstract/Summary:PDF Full Text Request
[Background]Despite considerable progress in understanding pathophysiology of pancreatitis, the mechanisms of the development of this disease remain obscure. Over the past several years, evidence has been accumulating on the involvement of inflammatory mediators, such as cytokines- Chemokines interleukin-1(IL-1),IL-6,IL-8,tumor necrosis factor-a (TNF- a),and platelet-activating factor(PAF), in the development of pancreatitis. Systemic levels of IL-6,IL-8 and TNF- a increase in patients with acute pancreatitis and correlate with the severity of the disease.A key regulator of cytokine induction is the pleiotropic transcription factor nuclear factor-κB. NF-κB represents a family of proteins sharing the Rel homology domain, which bind to DNA as homoor heterodimers, and activate a multitude of cellular stress-related and early response genes such as the genes for cytokines, growth factors, adhesion molecules, and acute phase proteins. NF-κB plays an important role in some severs inflammatory diseases and gastrointestinal tumors.[Purpose] To investigate the effects and mechanism of Emodin in severe acute pancreatitis (SAP) and severe acute pancreatitis (SAP) associated acute lung injury (ALI).[Method] A total of thirty Sprague-Dawley rats were randomly divided into sham operation group, SAP group and Emodin treatment group. The model of SAP was established by retrograde pancreatic injection of sodium taurocholate(1ml/kg). Intrapulmonary and intrapancreate expression of NF-κB was assayed by streptavidin peroxidase conjugated method(SP). Meanwhile, serum level of amylase, ascites volume, pulmonary and pancreatic wet/dry ratio and pulmonary and pancreatic histological grading were also measured.[Results] 1. The influence of ascites volume AMS level pancreatic and pulmonary wet/dry weight ratio by Emodin: The ascites volume AMS level pancreatic and pulmonary wet/dry weight ratio of pancreatic group was remarkably higher than the sham operation group , the ascites volume AMS level pancreatic and pulmonary wet/dry weight ratio of Emodin treatment group was higher than the sham operation group, but it was much lower than SAP group. (P all <0.01)2. The influence of pulmonary and pancreatic histological grading: No obvious pathological changes were found in pancreatic and pulmonary tissue of sham operation group under microscope, but it could be found in SAP group. There weren't obvious pathological changes in pulmonary tissue of Emodin treatment group, pathological injuries of pancreas in Emodin treatment group were significantly less than in SAP group (P <0.01) .3. The influence of the expressions of NF-κB by Emodin: The expressions of NF-κB in pancreatic and pulmonary tissues could hardly be found in sham operation group . In SAP group and Emodin treatment group, the expressions of NF-κB in pancreatic and pulmonary tissues remarkably increased compared to those in sham operation group (all P <0.01) ,and they decreased much more in Emodin treatment group than that in SAP group (P <0.01) .[Conclusion] Emodin plays a role in the treatment of SAP and SAP associated ALI. It may depress the expression of NF-κB and suppress the inflammatory response of pancreatic and pulmonary tissues.
Keywords/Search Tags:Pancreatitis, Lung injury, Nuclear factor-kappa B, Emodin
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