Beneficial effects of angiotensin converting enzyme inhibitors captopril and enalapril on experimentally induced colitis in rats

Increasing evidence supports an association between inflammation and angiotensin converting enzyme [ACE]. The aim of this study was to examin the efficacy of ACE inhibitors [ACEIs] namely, captopril and enalapril on acetic acid induced colitis in rats. Colitis was induced by intracolonic injection of 2 ml of 3% acetic acid. Eighty rats were studied in this study, divided into: two main groups, group 1, 40 rats of long duration of inflammation and treatment and group II, 40 rats of short duration of inflammation and treatment. Each group was subdivided into 4 subgroups. 10 control rats, 10 rats injected intracolonic with acetic acid [acetic acid untreated rats], 10 rats injected intracolonic with acetic and plus oral administration of captopril [captopril treated rats], and 10 rats injected intracolonic with acetic acid plus oral administration of enalapril [enalapril treated rats]. Captopril and enalapril were given 2 days after induction of colitis and continued daily for 3 weeks in group I, and for 2 days before and 2 days after induction of colitis in group II. Intracolonic acetic acid injection produced a significant inflammation, assessed by the ulcer index score, the weight of the colon and the colonic tissue level of myeloperoxidase enzyme, in acetic acid untreated rats of both groups. These parameters were significantly improved by ACEIs administration. The effect of captopril in group I was more potent than enalapril, while in group II both ACEIs had the same effect. in group II captopril succeeded to inhibit the change in the weight of the colon or the tissue level of myeloperoxidase enzyme. The colonic tissue level of glutathione reductase was significantly reduced in acetic acid untreated rats of both groups. This reduction was significantly inhibited by ACEIs administration in both groups, with better results with captopril treated rats than enalapril ones in group I. Also the efficacy of captopril in group I was more significant than in group II in improving the glutathione reductase colonic tissue level. Captopril and enalapril also sigificantly improved the level of tissue lipid peroxides, which was significantly elevated in acetic acid untreated rats of both groups. However, the efficiency of captopril in reducing the lipid peroxides level was mor significant than enalapril in both groups. this study provides an evidence that the two ACEIs particularly captopril confers a good anti-inflammatory activity against colitis in rats leading to improvement of oxidative stress induced by the inflammatory insult

study of the potential role of aldose reductase inhibitors [Sorbinil, Tolrestat and Ponalrestat] in the amelioration of nephropathy in diabetic rats

This work included 90 male albino rats. Diabetes was induced by a single intraperitoneal injection of streptozotocin [STZ] in a dose of 55 mg/kg body weight. One week after STZ injection, uninephrectomy was done and the study began one week after uninephrectomy operation and continued for eight months. The results revealed that oral administration of sorbinil, tolrestat or ponalrestat for eight months in uninephrectomized [UNE] diabetic rats produced significant decreases in sorbitol and fructose levels in RBCs, kidney sorbitol and aldose reductase activity in RBCs associated with significant increases in Na

comparative study between gliclazide, glibenclamide and glipizide on plasma glucose, C-peptide, lipid profile and on some peroxidative changes in diabetic rats

This study was performed on 50 male adult albino rats [10 normal and 40 alloxan-induced diabetic rats] divided into five groups, each of ten rats. The study recommended the use of gliclazide in NIDDM due to its excellent glycemic control and prevention of the long- term vascular complications; it also restores the abnormalities in lipid peroxides, oxidative markers and antioxidant enzymes

Do all calcium antagonists have a cardioprotective effect against isoproterenol induced myocardial necrosis in rats?

This study investigated and compared the possible protective effects of five Ca2+ entry blockers: Verapamil, nifedipine, diltiazem, flunarizine and amlodipine against isoproterenol-induced myocardial necrosis in rats. Fifty-six male albino rats were divided into seven equal groups. Group 1 served as control, group 2 received isoproterenol [85 mg/kg body wt. s.c.] for two days to produce myocardial necrosis, other groups received one of the following Ca2+ entry blockers for four successive days: verapamil [5 mg/kg body weight i.p.], nifedipine [0.2 mg/kg i.m.], diltiazem [10 mg/kg i.m.], flunarizine [30 mg/kg orally] and amlodipine [0.5 mg/kg orally]. On the third and fourth days of treatment, animals received isoproterenol in the dose mentioned above. Twenty-four hours later, blood samples were withdrawn from the orbital plexus for the determination of creatine phosphokinase [CPK] activity, aspartate aminotransferase [ASAT] and alanine aminotransferase [ALAT]. The post-ischemic survival rate [PISR] for each group was calculated. Isoproterenol caused a significant increase in CPK, ASAT and ALAT as compared to the control group, the PISR was 0%. Pretreatment with nifedipine, verapamil or diltiazem significantly reduced all the enzyme studied as compared to isoproterenol group, the PISR was 87.5% 75% and 75%, respectively. Amlodipine pretreatment reduced only ASAT, PISR was 25%. On the other hand, flunarizine pretreatment did not significantly change the enzyme studied, the PISR was 12.5%. The results suggested that nifedipine, verapamil and diltiazem have protective effects against isoproterenol-induced myocardial necrosis in rats and that flunarizine and amlodipine were free of these cardioprotective effects