Dissertation > Medicine, health > Internal Medicine > Digestive and abdominal diseases > Liver and gall bladder disease > Cirrhosis

Expression of SGK1 in Hepatic Fibrosis Rats and Its Intervention by Candesartan

Author ZhangShuJing
Tutor ShiShuiSheng
School Shanxi Medical
Course Department of Gastroenterology,
Keywords Hepatic fibrosis SGK1 Candesartan
CLC R575.2
Type Master's thesis
Year 2011
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Objective:To study the expression of serum and glucocorticoid regulated protein kinase 1(SGK1),and its intervention by selective angiotensinⅡreceptor ATl antagonist candesartan inhepatic fibrosis rats,and to clarify the relationship between SGK1 and hepatic fibrogenesis,providing the laboratory basis for the diagnosis of liver fibrosis.Methods:36 Wistar rats were randomly divided into the following groups:normalcontrols,hepatic fibrosis models,rats treated with candesartan,starting at the seventh week sincethe rats exposed to composite factors.All rats were sacrificed and their livers were collected forfurther determinations at the corresponding week.The liver histopathology was examined by HEand Masson staining.The expressions and sites of SGK1、α-SMA and TGF-β1 in liver tissuewere also detected by immunohistochemical staining,and the semi-quantitative analysis of thepositive expression was carried out through the imagine analysis system.Results:Hepatic fibrosis model was induced successfully by composite factors.At the sixthweek,the structure of hepatic cords in hepatic fibrosis models was destroyed,part ofhepatocytes were degenerated and necrotized,there is statistic significance compared with thenormal controls on the percentage of the area of collage (p<0.01);The collagen in the liverprolif-erates obviously both at the eighth week and at the tenth week,the percentage of the areaof collage was significantly increased compared with the normal controls (p<0.01);There arestatistic significances among each model group on the percentage of the area of collage(p<0.05);At the eighth week and tenth week,the percentage of the area of collage weredecreased in rats treated with Candesartan compared with the corresponding model rats (p均<0.05);but there is no significance between two Candesartan groups (p>0.05).With thedevelopment of liver fibrosis,the expressions of SGK1,TGF-β1,α-SMA in liver tissue wereincreased gradually,and there is significance not only between each model group and normalcontrols but also among each model group(p均<0.05).At the eighth and tenth week,expressions of SGK1,TGF-β1,α-SMA were remarkably decreased in rats treated withCandesartan compared with the corresponding modelrats (p均<0.05);Compared with the eighthweek,expression ofα-SMA in rats treated with Candesartan at the tenth week were notsignificantly changed(p>0.05),but the ex-pressions of SGK1,TGF-β1 in liver tissue weredecreased(p< 0.05).The expression of SGK1 in liver tissue is relative both to the expression ofTGF-β1 significantly( r=0.957,p< 0.05)),and to the expression ofα-SMA in liver tissue (r =0.899,p <0.001).Conclution: With the development of liver fibrosis,the expression of SGK1 was increased,indicating that SGK1 involves in the hepatic fibrogenesis.The expression of SGK1 inliver tissue is positive correlated both to the expression of TGF-β1 and to the expression ofα-SMA.When treated with Candesartan,expression of SGK1 were decreased gradually and thedegree of hepatic fibrosis was reduced.The mechanism may be associated with the effect ofdown-regulating TGF-β1 and then resulting in suppressing the activation of hepatic stellatecells.

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