N-acetylcysteine and intestinal health: a focus on its mechanism of action.
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abstract
The integrity of the intestinal epithelium ensures its normal physiological function. Consequently, damage to the mucosal epithelium can impair the absorption of nutrients, thereby reducing the growth performance and compromising the health of animals. N-acetylcysteine (NAC) is pharmaceutically available either intravenously, orally, or by inhalation for reducing endothelial dysfunction, inflammation, fibrosis, invasion, cartilage erosion, acetaminophen detoxification, and transplant prolongation. NAC is rapidly metabolized by the small intestine to produce glutathione and can not be detected in animals without supplementation. The physiologic functions and therapeutic effects of NAC are largely associated with maintaining intracellular concentrations of reduced glutathione. Results from recent studies indicate that NAC reduces inflammation, alleviates oxidative stress, improves energy status, and ameliorates tissue damage in the intestine of lipopolysaccharide-challenged piglets. Moreover, dietary supplementation with NAC ameliorates acetic acid-induced colitis in a porcine model. The effects of NAC are associated with some intestinal cell signaling pathways, such as EGFR, TLR4, apoptosis and tight junction signaling. The current review focuses on the protective effects of NAC on intestinal health and the molecular mechanisms of its action.
