N-acetylcysteine reduces inflammation in the small intestine by regulating redox, EGF and TLR4 signaling

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• 作者：Yongqing Hou (1)
  Lei Wang (1)
  Dan Yi (1)
  Binying Ding (1)
  Zhenguo Yang (1)
  Jiao Li (1)
  Xing Chen (1)
  Yinsheng Qiu (1)
  Guoyao Wu (2) (3)
  
• 关键词：N ; acetylcysteine ; Intestinal mucosa ; Lipopolysaccharide ; Epidermal growth factor ; Toll like receptor ; Aquaporin
• 刊名：Amino Acids
• 出版年：2013
• 出版时间：September 2013
• 年：2013
• 卷：45
• 期：3
• 页码：513-522
• 全文大小：389KB
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• 作者单位：Yongqing Hou (1)
  Lei Wang (1)
  Dan Yi (1)
  Binying Ding (1)
  Zhenguo Yang (1)
  Jiao Li (1)
  Xing Chen (1)
  Yinsheng Qiu (1)
  Guoyao Wu (2) (3)
  
  1. Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, 430023, Wuhan, China
  2. State Key Laboratory of Animal Nutrition, China Agricultural University, 100193, Beijing, China
  3. Department of Animal Science, Texas A&M University, College Station, TX, 77843, USA
  

文摘

This study determined whether N-acetylcysteine (NAC) could affect intestinal redox status, proinflammatory cytokines, epidermal growth factor (EGF), EGF receptor (EGFR), Toll-like receptor-4 (TLR4), and aquaporin-8 in a lipopolysaccharide (LPS)-challenged piglet model. Eighteen piglets (35-day-old) were randomly allocated into one of the three treatments (control, LPS and NAC). The control and LPS groups were fed a basal diet, and the NAC group received the basal diet +500?mg/kg NAC. On days 10, 13, and 20 of the trial, the LPS- and NAC-treated piglets received intraperitoneal administration of LPS (100?μg/kg BW), whereas the control group received the same volume of saline. On days 10 and 20, venous blood samples were obtained at 3?h post LPS or saline injection. On day 21 of the trial, piglets were killed to obtain the intestinal mucosa for analysis. Compared with the control group, LPS challenge reduced (P?<?0.05) the activities of superoxide dismutase, catalase, and glutathione peroxidase in jejunal mucosae, while increasing (P?<?0.05) the concentrations of malondialdehyde, H2sub>O2sub>, O2sub> ·?/sup> and the ratio of oxidized to reduced glutathione in jejunal mucosae, and concentrations of TNF-α, cortisol, interleukin-6, and prostaglandin E2sub> in both plasma and intestinal mucosae. These adverse effects of LPS were attenuated (P?<?0.05) by NAC supplementation. Moreover, NAC prevented LPS-induced increases in abundances of intestinal HSP70 and NF-κB p65 proteins and TLR4 mRNA. NAC supplementation enhanced plasma EGF concentration and intestinal EGFR mRNA levels. Collectively, these results indicate that dietary NAC supplementation alleviates LPS-induced intestinal inflammation via regulating redox, EGF, and TLR4 signaling.