The Healing Process of Chronic Colitis in Rats, Induced by 2,4,6-Trinitrobenzene Sulfonic Acid, with Special Reference to the Role of Fibronectin

During inflammatory colitis in man and experimental animals, the production of free radicals increases. This study evaluated the histological pattern and biochemical parameters of oxidative damage during acute and chronic colitis induced by 2,4,-trinitrobenzenesulfonic acid + ethanol in rats. On the samples of scraped mucosa of six groups of rats, one not treated, one killed after 1 hr, and those killed one, two, four, and eight weeks after the induced-damage, we determined the histological and superoxide dismutase activity and the concentration of lipoperoxides, malonyldialdheyde, and reduced glutathione. After 1 hr, the mucosal damage and superoxide dismutase activity were slight; glutathione, lipoperoxides, and malonyldialdheyde were significantly increased. At one week, the histological damage was severe, decreasing progressively, and significantly correlated to superoxide dismutase activity. Lipoperoxides and malonyldialdheyde were high throughout the study. Glutathione was significantly increased at one and two weeks and dramatically decreased thereafter. Therefore, in experimental colitis the cascade of free-radical production induces a constant self-maintaining lipoperoxidation and consumes the cellular antioxidant capability.

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The Healing Process of Chronic Colitis in Rats, Induced by 2,4,6-Trinitrobenzene Sulfonic Acid, with Special Reference to the Role of Fibronectin

Abstract: These observations elucidate the role of young fibroblasts, as multipotent cells, and of fibronectin in acceleration of the healing process in this model of chronic colitis.

Cited by 7 publications

References 18 publications

Application of recombinant DNA technology to the identification of novel therapeutic targets in inflammatory bowel disease

Application of recombinant DNA technology to the identification of novel therapeutic targets in inflammatory bowel disease

Kupffer cells and endothelial cells

Direct evidence of oxidative damage in acute and chronic phases of experimental colitis in rats

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