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Intestinal smooth muscle dysfunction after intraperitoneal injection of zymosan in the rat: are oxygen radicals
A van der Vliet1, K I van der Poel, A Bast
1Department of Pharmacochemistry, Faculty of Chemistry, Vrije Universiteit, Amsterdam, The Netherlands.
Abstract:
Zymosan is frequently used as an activator of granulocytes to study inflammatory responses. We used zymosan as a model to understand the mechanisms involved in intestinal inflammatory diseases, and our special interest was focused on the smooth muscle function. Moreover, we investigated the role of oxidative stress in intestinal pathology after inflammatory processes. Intraperitoneal injection of zymosan induces a peritoneal inflammation, characterised by exudate in the peritoneum and peritoneal fibrosis. Three days after injection of zymosan (25-40 mg/100 g) we measured a decreased beta adrenergic smooth muscle response, while the muscarinic receptor-mediated contraction was not significantly affected. Efforts were made to correlate these observations with the development of oxidative stress; however, the intestinal glutathione balance remained undisturbed and no increase in lipid peroxidation products in the intestine was observed. Our conclusion is the peritoneal inflammation will lead to a release of various mediators, which may destroy receptor systems, among which are beta adrenoceptors. There was no evidence of an important role for reactive oxygen metabolites in this effect.
Insights
Zymosan-induced inflammation in mice impairs beta-adrenergic smooth muscle response in the intestine. This study found no evidence that oxidative stress contributes to this inflammatory effect on intestinal smooth muscle function.
Area of Science:
- Gastroenterology
- Immunology
- Pharmacology
Background:
- Zymosan is a common activator of granulocytes used to model inflammatory responses.
- Intestinal inflammatory diseases can significantly impact smooth muscle function.
- Oxidative stress is implicated in various pathological conditions.
Purpose of the Study:
- To investigate the effects of zymosan-induced peritoneal inflammation on intestinal smooth muscle function.
- To explore the role of oxidative stress in the observed intestinal pathology.
- To understand the mechanisms underlying smooth muscle dysfunction during inflammation.
Main Methods:
- Intraperitoneal injection of zymosan in mice to induce peritoneal inflammation and fibrosis.
- Measurement of smooth muscle responses mediated by beta-adrenergic and muscarinic receptors.
- Assessment of oxidative stress markers, including glutathione balance and lipid peroxidation products.
Main Results:
- Zymosan injection led to peritoneal exudate and fibrosis.
- A significant decrease in beta-adrenergic smooth muscle response was observed three days post-injection.
- Muscarinic receptor-mediated contraction remained unaffected.
- No significant alterations in intestinal glutathione balance or lipid peroxidation were detected.
Conclusions:
- Peritoneal inflammation induced by zymosan can lead to the release of mediators that impair beta-adrenoceptor function in the intestine.
- Reactive oxygen metabolites do not appear to play a significant role in the observed smooth muscle dysfunction.
- The findings suggest a specific impact on adrenergic signaling pathways during inflammation.
