Protective effect of exogenous nitrite in postoperative ileus
S M R Cosyns1, S Shiva2,3,4, R A Lefebvre1
1Heymans Institute of Pharmacology, Ghent University, Ghent, Belgium.
British Journal of Pharmacology
|August 1, 2015
Summary
Sodium nitrite administration improved intestinal transit and contractility in a mouse model of postoperative ileus (POI). This protective effect involved nitric oxide (NO) and soluble guanylyl cyclase activation, not mitochondrial complex I inhibition.
Area of Science:
- Gastroenterology
- Pharmacology
- Physiology
Background:
- Postoperative ileus (POI) pathogenesis involves inflammation and oxidative stress.
- Nitrite can ameliorate ischemia/reperfusion injury, suggesting potential therapeutic roles.
Purpose of the Study:
- To investigate nitrite's protective effects against POI in a mouse model.
- To elucidate the underlying mechanisms of nitrite's action in POI.
Main Methods:
- Intestinal manipulation (IM) induced POI in C57BL/6J mice.
- Sodium nitrite was administered intravenously before IM.
- Intestinal transit, contractility, inflammatory markers, iNOS, ROS, mitochondrial complex I, and cGMP were assessed.
Main Results:
- Nitrite significantly improved intestinal transit and restored contractility post-IM.
- Nitrite reduced TNF-α, IL-6, CCL2, iNOS activity, and ROS levels.
- Nitrite increased cGMP levels; protective effects were abolished by NO scavenger or guanylyl cyclase inhibitor.
Conclusions:
- Exogenous nitrite shows promise as a potential POI treatment.
- Nitrite's protective effects in POI are NO-dependent and involve soluble guanylyl cyclase activation.
- The mechanism does not involve inhibition of mitochondrial complex I.
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