Protective effects of N-acetylcysteine on acetic acid-induced colitis in a porcine model

• Published in: BMC gastroenterology 2013-08, Vol.13 (1), p.133-133, Article 133
• Main Authors: Wang, Qingjing, Hou, Yongqing, Yi, Dan, Wang, Lei, Ding, Binying, Chen, Xing, Long, Minhui, Liu, Yulan, Wu, Guoyao
• Format: Article
• Language: English
• Subjects: Acetic Acid; Acetylcysteine; Acetylcysteine - pharmacology; Acetylcysteine - therapeutic use; Amphiregulin; Analysis; Animals; Apoptosis - drug effects; Caspase 3 - drug effects; Caspase 3 - metabolism; Claudin-1 - drug effects; Claudin-1 - metabolism; Colitis; Colitis - chemically induced; Colitis - pathology; Colitis - prevention & control; Colitis, Ulcerative; Colon; Colon - drug effects; Colon - metabolism; Colon - pathology; Cytokines; Diet; Dietary Supplements; Dinoprostone - metabolism; Disease Models, Animal; EGF Family of Proteins; Epidermal growth factor; Epidermal Growth Factor - blood; Epidermal Growth Factor - drug effects; Free Radical Scavengers - pharmacology; Free Radical Scavengers - therapeutic use; Gastroenterology; Glycoproteins - drug effects; Glycoproteins - genetics; Histochemistry; Hogs; Inflammatory bowel disease; Intercellular Signaling Peptides and Proteins - genetics; Interleukin-6 - metabolism; Intestinal Mucosa - drug effects; Intestinal Mucosa - metabolism; Intestinal Mucosa - pathology; Receptor, Epidermal Growth Factor - drug effects; Receptor, Epidermal Growth Factor - genetics; RNA; Swine; Toll-Like Receptor 4 - drug effects; Toll-Like Receptor 4 - genetics; Transforming Growth Factor alpha - drug effects; Transforming Growth Factor alpha - metabolism; Tumor Necrosis Factor-alpha - drug effects; Tumor Necrosis Factor-alpha - genetics; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 1471-230X; 1471-230X
• DOI: 10.1186/1471-230X-13-133

Ulcerative colitis is a chronic inflammatory disease and involves multiple etiological factors. Acetic acid (AA)-induced colitis is a reproducible and simple model, sharing many characteristics with human colitis. N-acetylcysteine (NAC) has been widely used as an antioxidant in vivo and in vitro. NAC can affect several signaling pathways involving in apoptosis, angiogenesis, cell growth and arrest, redox-regulated gene expression, and inflammatory response. Therefore, NAC may not only protect against the direct injurious effects of oxidants, but also beneficially alter inflammatory events in colitis. This study was conducted to investigate whether NAC could alleviate the AA-induced colitis in a porcine model. Weaned piglets were used to investigate the effects of NAC on AA-induced colitis. Severity of colitis was evaluated by colon histomorphology measurements, histopathology scores, tissue myeloperoxidase activity, as well as concentrations of malondialdehyde and pro-inflammatory mediators in the plasma and colon. The protective role of NAC was assessed by measurements of antioxidant status, growth modulator, cell apoptosis, and tight junction proteins. Abundances of caspase-3 and claudin-1 proteins in colonic mucosae were determined by the Western blot method. Epidermal growth factor receptor, amphiregulin, tumor necrosis factor-alpha (TNF-α), and toll-like receptor 4 (TLR4) mRNA levels in colonic mucosae were quantified using the real-time fluorescent quantitative PCR. Compared with the control group, AA treatment increased (P