The effect of increasing amounts of a cyclic oligosaccharide, beta-cyclodextrin (BCD), included in the diet on plasma cholesterol and triglycerides, was investigated in two animal models, namely in male genetically hypercholesterolemic Rico rats and in male Syrian hamsters. The distribution of bile acids in the gastrointestinal tract and in the feces of hamsters was also determined. In the Rico rats and hamsters, plasma cholesterol and triglycerides decreased linearly with increasing doses of BCD. In these two species, 20% BCD as compared to control diet lowered cholesterolemia (-35%) and triglyceridemia (-70%). In the hamster, the BCD diet caused a marked decrease in cholesterol and triglycerides in chylomicrons and very low density lipoprotein, and in high density lipoproteins cholesterol. Composition and amounts of bile acids were modified in the gastrointestinal tract of hamsters receiving 10% BCD as compared to the control group. The total bile acid content of the gallbladder of treated hamsters was fourfold higher than in the control group, and the bile contained a large amount of hydrophilic bile acids. This trend was also observed in the small intestine, in which percentages and total quantities of cholic plus deoxycholic acids (cholic pathway) were higher than those of chenodeoxycholic plus ursodeoxycholic plus lithocholic acids (chenodeoxycholic pathway). The bile acid contents of the cecum and colon of treated hamsters were 2.7-fold higher than those of control animals, but the bile acid composition was similar in the two groups of hamsters.(ABSTRACT TRUNCATED AT 250 WORDS)
The role of gaseous mediators NO and H2S and the cyclooxygenase/prostaglandins system in large intestinal mucosa was investigated in experiments on white rats under condition of experimental ulcerative colitis caused by introduction of acetic acid. Ulcerative colitis was accompanied by the formation of lesions of mucosal barrier of large intestine and the presence of ulcerative defects. The administration of H2S-releasing compound ATB-346 on the background of colitis significantly decreases the area of lesions as compared to naproxen or celecoxib action, that is the most probably caused by the action of H2S. Nonselective cyclooxygenase inhibition by naproxen was accompanied by the decrease of H2S concentration in blood serum and the level of gene Cbs expression in large intestinal mucosa, whereas under the condition of АТВ-346 action the above parameters were close to their normal values. Both naproxen and АТВ-346 decreased the level of gene Nos2 expression and activity of iNOS, which was sharply increased in colitis. Thus, the action of the naproxen derivative H2S releasing compound АТВ-346 is mainly caused by the action of hydrogen sulfide and its influence on іNOS system, and is manifested by a better cytoprotective effect as compared to naproxen action on the background of experimental ulcerative colitis.
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