Angiotensin-Converting Enzyme Inhibition Attenuates the Progression of Rat Hepatic Fibrosis

Jonsson, Julie R.; Clouston, Andrew D.; Ando, Yumiko; Kelemen, L.; Horn, Murray J.; Adamson, Michael D.; Purdie, David M.; Powell, Elizabeth E.

doi:10.1053/gast.2001.25480

Cited by 271 publications

(215 citation statements)

References 30 publications

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“…Captopril improves insulin sensitivity, 41 has antioxidant properties, 42 and is able to scavenge reactive oxygen species 43 and to attenuate the progression of hepatic fibrosis in rats. 44 In our study, captopril did not significantly improve insulin resistance; however, there was a significant reduction in plasma and hepatic triglycerides, with a decrease in the macrovesicular steatosis score. Surprisingly, there was a mild increase in HIC, which was accompanied by an increase in the fibrosis score.…”

Section: Discussioncontrasting

confidence: 56%

Fructose-Induced Fatty Liver Disease

et al. 2005

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Abstract-The most known risk factor for nonalcoholic fatty liver disease (NAFLD) is the metabolic syndrome. In this study, we characterized changes in liver pathology, hepatic lipid composition, and hepatic iron concentration (HIC) occurring in rats given fructose-enriched diet (FED), with and without therapeutic maneuvers to reduce blood pressure and plasma triglycerides. Rats were given FED or standard rat chow for 5 weeks. Rats on FED were divided into 4 groups: receiving amlodipine (15 mg/kg per day), captopril (90 mg/kg per day), bezafibrate (10 mg/kg per day) in the last 2 weeks, or a control group that received FED only. FED rats had hepatic macrovesicular and microvesicular fat deposits develop, with increase in hepatic triglycerides (ϩ198%) and hepatic cholesterol (ϩ89%), but a decrease in hepatic phospholipids (Ϫ36%), hypertriglyceridemia (ϩ223%), and hypertension (ϩ15%), without increase in HIC. Amlodipine reduced blood pressure (Ϫ18%), plasma triglycerides (Ϫ12%), but there was no change in hepatic triglycerides and phospholipids concentrations. Captopril reduced blood pressure (Ϫ24%), plasma triglycerides (Ϫ36%), hepatic triglycerides (Ϫ51%), and hepatic macrovesicular fat (Ϫ51%), but increased HIC (ϩ23%), with a borderline increase in hepatic fibrosis. Bezafibrate reduced plasma triglycerides (Ϫ49%), hepatic triglycerides (Ϫ78%), hepatic macrovesicular fat (Ϫ90%), and blood pressure (Ϫ11%

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Section: Discussioncontrasting

confidence: 56%

Fructose-Induced Fatty Liver Disease

et al. 2005

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“…Similar results were obtained with antifibrotic agents, including inhibitors of angiotensin-converting enzyme. 43 Although the reason remains uncertain, these studies support the hypothesis that reduction of liver fibrosis limits cholestatic injury. 44 In conclusion, our study demonstrates that PAR 1 antagonism protects against fibrosis in a rodent model of liver injury.…”

Section: Discussionmentioning

confidence: 64%

PAR1 antagonism protects against experimental liver fibrosis. Role of proteinase receptors in stellate cell activation

et al. 2004

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In fibroblasts, thrombin induces collagen deposition through activation of a G-proteincoupled receptor, proteinase-activated receptor 1 (PAR 1 ). In the current study, we examined whether PAR 1 antagonism inhibits hepatic stellate cell (HSC) activation in vitro and whether it protects against fibrosis development in a rodent model of cirrhosis. A rat HSC line was used for in vitro studies whereas cirrhosis was induced by bile duct ligation (

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“…22 Hydroxyproline Hydroxyproline was measured using a colorimetric assay as previously described. 23,24 Briefly, 240-mg liver segments were hydrolyzed in HCl, to which 40 mg of Norit/Dowex mixture was added for 21 h at 1101C. Following centrifugation and filtration, the pH was adjusted.…”

Section: Grading Liver Fibrosis and Histologymentioning

confidence: 99%