title: The effect of angiotensin-converting enzyme inhibitors on experimental colitis in rats.
abstract: The present study was aimed to investigate the effect of ACE inhibition on trinitrobenzene sulphonic acid (TNBS)-induced colonic inflammation in rats by using captopril and lisinopril. In treatment groups, the rats were treated with ACE inhibitors, captopril or lisinopril (0.1 and 1 mg/kg/day; intraperitoneally). The drugs were given 5 min after induction of colitis and the treatment was continued for 3 days. Three days after the induction of colitis, all rats were decapitated. The distal colon was weighed and the mucosal lesions were scored at both macroscopical at microscopic levels. Malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were assessed in tissue samples. Formation of reactive oxygen species in colonic samples was monitored by using chemiluminescence technique. Serum TNF-alphalevel was assessed in trunk blood. Captopril treatment was found to be beneficial in all parameters, except colonic glutathione content. On the other hand, although stimulation of lipid peroxidation and increase in serum TNF-alpha level were successfully prevented by lisinopril, the morphology of the lesions remained unchanged. In conclusion, sulphydryl and non-sulphydryl ACE inhibitors, captopril and lisinopril do not seem to be similarly effective in TNBS-induced colitis model at least at the doses tested in our study.
authors.affiliation: Marmara University, School of Medicine, Department of Physiology, 34668 Haydarpasa, Istanbul, Turkey.
authors.forename: Nermina
authors.initials: N
authors.lastname: Jahovic
authors.forename: Feriha
authors.initials: F
authors.lastname: Ercan
authors.forename: Nursal
authors.initials: N
authors.lastname: Gedik
authors.forename: Meral
authors.initials: M
authors.lastname: Yüksel
authors.forename: Göksel
authors.initials: G
authors.lastname: Sener
authors.forename: Inci
authors.initials: I
authors.lastname: Alican
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D003092:Colitis / Q000188:drug therapy* / Q000201:enzymology*; D003094:Collagen / Q000378:metabolism; D003106:Colon / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005978:Glutathione / Q000378:metabolism; D017706:Lisinopril / Q000494:pharmacology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009929:Organ Size; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species; D013997:Time Factors; D014302:Trinitrobenzenesulfonic Acid / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004791:Enzyme Inhibitors; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D014302:Trinitrobenzenesulfonic Acid; D003094:Collagen; D002216:Captopril; D017706:Lisinopril; D009195:Peroxidase; D005978:Glutathione