2011Chinese Journal of Gastroenterology and HepatologyRequires access

Changes of sIgA of intestinal mucosal fluid in the progress of non-alcoholic steatohepatitis in rats

WU Wan-chun

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Abstract

Objective To explore the changes of sIgA of intestinal mucosal fluid and serum levels of endotoxin in the progress of non-alcoholic steatohepatitis(NASH) in rats.Methods Thirty-two SD rats were randomly divided into control group and model group.The rats in control group were fed with normal diet.The rats in model group were fed with fat-rich diet to establish the model of non-alcoholic steatohepatitis.The 8 rats in each group were killed at the end of 8th,12th week respectively.The serum level of endotoxin in portal vein and the level of sIgA in intestinal mucosal fluid were measured.The activity of SOD and the content of MDA in intestinal tissue were measured.And the serum levels of TG,TC,ALT and AST were observed.The pathology of liver was observed by HE stain.Results The serum levels of TC,ALT and AST were higher in model group than those in control group at 8,12th week.The pathology of liver represented simple fatty liver and steatohepatitis respectively.At the end of 8th week,there was no marked change in the levels of endotoxin and sIgA between model group and control group(P0.05).At the end of 12th week,serum level of endotoxin in model group was higher than that in control group(P0.05),the level of sIgA of intestinal macosal fluid in model group was lower than that in control group(P0.05).Serum level of endotoxin in portal vein had a negative correlation with the level of sIgA of intestinal mucosal fluid (r=-0.873,P0.05).Compared with control group,the content of MDA was increased and the activity of SOD was decreased in intestinal tissue in model group at 8,12th week(P0.05).Conclusion The level of sIgA of intestinal mucosal fluid is decreased in rats with NASH.It suggests that the intestinal mucosa immune barrier function destruction exists,and it is possible concerned with the intestinal lipid peroxidation upgraded,which may be one of important factors in the the pathogenesis and progress of NASH.

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Objective To explore the changes of sIgA of intestinal mucosal fluid and serum levels of endotoxin in the progress of non-alcoholic steatohepatitis(NASH) in rats.Methods Thirty-two SD rats were randomly divided into control group and model group.The rats in control group were fed with normal diet.The rats in model group were fed with fat-rich diet to establish the model of non-alcoholic steatohepatitis.The 8 rats in each group were killed at the end of 8th,12th week respectively.The serum level of endotoxin in portal vein and the level of sIgA in intestinal mucosal fluid were measured.The activity of SOD and the content of MDA in intestinal tissue were measured.And the serum levels of TG,TC,ALT and AST were observed.The pathology of liver was observed by HE stain.Results The serum levels of TC,ALT and AST were higher in model group than those in control group at 8,12th week.The pathology of liver represented simple fatty liver and steatohepatitis respectively.At the end of 8th week,there was no marked change in the levels of endotoxin and sIgA between model group and control group(P0.05).At the end of 12th week,serum level of endotoxin in model group was higher than that in control group(P0.05),the level of sIgA of intestinal macosal fluid in model group was lower than that in control group(P0.05).Serum level of endotoxin in portal vein had a negative correlation with the level of sIgA of intestinal mucosal fluid (r=-0.873,P0.05).Compared with control group,the content of MDA was increased and the activity of SOD was decreased in intestinal tissue in model group at 8,12th week(P0.05).Conclusion The level of sIgA of intestinal mucosal fluid is decreased in rats with NASH.It suggests that the intestinal mucosa immune barrier function destruction exists,and it is possible concerned with the intestinal lipid peroxidation upgraded,which may be one of important factors in the the pathogenesis and progress of NASH.

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Available abstract

Objective To explore the changes of sIgA of intestinal mucosal fluid and serum levels of endotoxin in the progress of non-alcoholic steatohepatitis(NASH) in rats.Methods Thirty-two SD rats were randomly divided into control group and model group.The rats in control group were fed with normal diet.The rats in model group were fed with fat-rich diet to establish the model of non-alcoholic steatohepatitis.The 8 rats in each group were killed at the end of 8th,12th week respectively.The serum level of endotoxin in portal vein and the level of sIgA in intestinal mucosal fluid were measured.The activity of SOD and the content of MDA in intestinal tissue were measured.And the serum levels of TG,TC,ALT and AST were observed.The pathology of liver was observed by HE stain.Results The serum levels of TC,ALT and AST were higher in model group than those in control group at 8,12th week.The pathology of liver represented simple fatty liver and steatohepatitis respectively.At the end of 8th week,there was no marked change in the levels of endotoxin and sIgA between model group and control group(P0.05).At the end of 12th week,serum level of endotoxin in model group was higher than that in control group(P0.05),the level of sIgA of intestinal macosal fluid in model group was lower than that in control group(P0.05).Serum level of endotoxin in portal vein had a negative correlation with the level of sIgA of intestinal mucosal fluid (r=-0.873,P0.05).Compared with control group,the content of MDA was increased and the activity of SOD was decreased in intestinal tissue in model group at 8,12th week(P0.05).Conclusion The level of sIgA of intestinal mucosal fluid is decreased in rats with NASH.It suggests that the intestinal mucosa immune barrier function destruction exists,and it is possible concerned with the intestinal lipid peroxidation upgraded,which may be one of important factors in the the pathogenesis and progress of NASH.

Key concepts: Steatohepatitis, Internal medicine, Fatty liver, Medicine, Gastroenterology, Portal vein, Endocrinology, Disease

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