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פותח על ידי קלירמאש פתרונות בע"מ -
Losartan reduces trinitrobenzene sulphonic acid-induced colorectal fibrosis in rats
Year:
2012
Authors :
פינס, מרק
;
.
Volume :
26
Co-Authors:
Wengrower, D., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Zanninelli, G., Gastroenterology Unit, Department of Internal Medicine and Public Health, University of l'Aquila, L'Aquila, Italy
Latella, G., Gastroenterology Unit, Department of Internal Medicine and Public Health, University of l'Aquila, L'Aquila, Italy
Necozione, S., Clinical Epidemiology Unit, Department of Internal Medicine and Public Health, University of l'Aquila, L'Aquila, Italy
Metanes, I., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Israeli, E., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Lysy, J., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Pines, M., Institute of Animal Science, Volcani Center, Bet Dagan, Israel
Papo, O., Department of Pathology, Hadassah University Hospital, Jerusalem, Israel
Goldin, E., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Facilitators :
From page:
33
To page:
39
(
Total pages:
7
)
Abstract:
BACKGROUND: Intestinal fibrosis is a challenging clinical condition in several fibrostenosing enteropathies, particularly Crohn's disease. Currently, no effective preventive measures or medical therapies are available for intestinal fibrosis. Fibrosis, due to an abnormal accumulation of extracellular matrix proteins, is a chronic and progressive process mediated by cell/matrix/cytokine and growth factor interactions, but may be a reversible phenomenon. Of the several molecules regulating fibrogenesis, transforming growth factor-beta 1 (TGF-β1) appears to play a pivotal role; it is strongly induced by the local activation of angiotensin II. The levels of both TGF-β1 and angiotensin II are elevated in fibrostenosing Crohn's disease. AIMS: To evaluate the in vivo effect of losartan - an angiotensin II receptor antagonist - on the course of chronic colitis-associated fibrosis and on TGF-β1 expression. METHODS: Colitis was induced by intrarectal instillation of trinitrobenzene sulphonic acid (TNBS) (15 mg/mL) while losartan was administered orally daily by gavage (7 mg/kg/day) for 21 days. Three groups of rats were evaluated: control (n=10); TNBS treated (n=10); and TNBS + losartan treated (n=10). Inflammation and fibrosis of the colon were evaluated by macro- and microscopic score analysis. Colonic TGF-β1 levels was measured using ELISA. RESULTS: Twenty-one days after induction, losartan significantly improved the macro- and microscopic scores of fibrosis in the colonic wall and reduced TGF-β1 concentration. CONCLUSIONS: Prophylactic oral administration of losartan reduces the colorectal fibrosis complicating the TNBS-induced chronic colitis, an effect that appears to be mediated by a downregulation of TGF-β1 expression. ©2012 Pulsus Group Inc. All rights reserved.
Note:
Related Files :
animal experiment
animal model
Animals
animal tissue
intestine wall
Male
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More details
DOI :
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
22301
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:50
Scientific Publication
Losartan reduces trinitrobenzene sulphonic acid-induced colorectal fibrosis in rats
26
Wengrower, D., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Zanninelli, G., Gastroenterology Unit, Department of Internal Medicine and Public Health, University of l'Aquila, L'Aquila, Italy
Latella, G., Gastroenterology Unit, Department of Internal Medicine and Public Health, University of l'Aquila, L'Aquila, Italy
Necozione, S., Clinical Epidemiology Unit, Department of Internal Medicine and Public Health, University of l'Aquila, L'Aquila, Italy
Metanes, I., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Israeli, E., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Lysy, J., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Pines, M., Institute of Animal Science, Volcani Center, Bet Dagan, Israel
Papo, O., Department of Pathology, Hadassah University Hospital, Jerusalem, Israel
Goldin, E., Institute of Gastroenterology, Hadassah University Hospital, Hebrew University, PO Box 12000-Kyriat Hadassah, Jerusalem 91120, Israel
Losartan reduces trinitrobenzene sulphonic acid-induced colorectal fibrosis in rats
BACKGROUND: Intestinal fibrosis is a challenging clinical condition in several fibrostenosing enteropathies, particularly Crohn's disease. Currently, no effective preventive measures or medical therapies are available for intestinal fibrosis. Fibrosis, due to an abnormal accumulation of extracellular matrix proteins, is a chronic and progressive process mediated by cell/matrix/cytokine and growth factor interactions, but may be a reversible phenomenon. Of the several molecules regulating fibrogenesis, transforming growth factor-beta 1 (TGF-β1) appears to play a pivotal role; it is strongly induced by the local activation of angiotensin II. The levels of both TGF-β1 and angiotensin II are elevated in fibrostenosing Crohn's disease. AIMS: To evaluate the in vivo effect of losartan - an angiotensin II receptor antagonist - on the course of chronic colitis-associated fibrosis and on TGF-β1 expression. METHODS: Colitis was induced by intrarectal instillation of trinitrobenzene sulphonic acid (TNBS) (15 mg/mL) while losartan was administered orally daily by gavage (7 mg/kg/day) for 21 days. Three groups of rats were evaluated: control (n=10); TNBS treated (n=10); and TNBS + losartan treated (n=10). Inflammation and fibrosis of the colon were evaluated by macro- and microscopic score analysis. Colonic TGF-β1 levels was measured using ELISA. RESULTS: Twenty-one days after induction, losartan significantly improved the macro- and microscopic scores of fibrosis in the colonic wall and reduced TGF-β1 concentration. CONCLUSIONS: Prophylactic oral administration of losartan reduces the colorectal fibrosis complicating the TNBS-induced chronic colitis, an effect that appears to be mediated by a downregulation of TGF-β1 expression. ©2012 Pulsus Group Inc. All rights reserved.
Scientific Publication
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