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

Wang, Qingjing; Hou, Yongqing; Yi, Dan; Wang, Lei; Ding, Biao; Chen, Xing; Long, Minhui; Liu, Yulan; Wu, Guoyao

doi:10.1186/1471-230x-13-133

Cited by 58 publications

(50 citation statements)

References 66 publications

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“…Although GSH is known to be important for intestinal function (Mårtensson et al 1990;Wu et al 2004), emerging evidence indicates that NAC may protect intestinal cells from oxidative injury and apoptosis (Hou et al 2012;Zhu et al 2013). At present, there are no studies regarding effects of NAC on protein turnover (synthesis and degradation) in any cell type, although we demonstrated that NAC enhanced intestinal mucosal growth and improved intestinal function under lipopolysaccharide or acetic acid challenges (Hou et al 2012;Wang et al 2013).…”

Section: Introductionmentioning

confidence: 67%

N-acetylcysteine stimulates protein synthesis in enterocytes independently of glutathione synthesis

et al. 2015

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Dietary supplementation with N-acetylcysteine (NAC) has been reported to improve intestinal health and treat gastrointestinal diseases. However, the underlying mechanisms are not fully understood. According to previous reports, NAC was thought to exert its effect through glutathione synthesis. This study tested the hypothesis that NAC enhances enterocyte growth and protein synthesis independently of cellular glutathione synthesis. Intestinal porcine epithelial cells were cultured for 3 days in Dulbecco's modified Eagle medium containing 0 or 100 μM NAC. To determine a possible role for GSH (the reduced form of glutathione) in mediating the effect of NAC on cell growth and protein synthesis, additional experiments were conducted using culture medium containing 100 μM GSH, 100 μM GSH ethyl ester (GSHee), diethylmaleate (a GSH-depletion agent; 10 μM), or a GSH-synthesis inhibitor (buthionine sulfoximine, BSO; 20 μM). NAC increased cell proliferation, GSH concentration, and protein synthesis, while inhibiting proteolysis. GSHee enhanced cell proliferation and GSH concentration without affecting protein synthesis but inhibited proteolysis. Conversely, BSO or diethylmaleate reduced cell proliferation and GSH concentration without affecting protein synthesis, while promoting protein degradation. At the signaling level, NAC augmented the protein abundance of total mTOR, phosphorylated mTOR, and phosphorylated 70S6 kinase as well as mRNA levels for mTOR and p70S6 kinase in IPEC-1 cells. Collectively, these results indicate that NAC upregulates expression of mTOR signaling proteins to stimulate protein synthesis in enterocytes independently of GSH generation. Our findings provide a hitherto unrecognized biochemical mechanism for beneficial effects of NAC in intestinal cells.

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Section: Introductionmentioning

confidence: 67%

N-acetylcysteine stimulates protein synthesis in enterocytes independently of glutathione synthesis

et al. 2015

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“…In the present study, CGA supplementation increased hepatic concentrations of glutathione, indicating that CGA can promote glutathione synthesis in the liver. Glutathione also protects the small intestine (Wu et al 2013a; Hou et al 2012, 2013) and the large intestine (Wang et al 2013a) from oxidative damage. We suggest that glutathione (reduced form) in serum may be a useful biomarker for the biological properties of CGA in vivo.…”

Section: Discussionmentioning

confidence: 99%

Metabolomic analysis of amino acid and energy metabolism in rats supplemented with chlorogenic acid

et al. 2014

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This study was conducted to investigate effects of chlorogenic acid (CGA) supplementation on serum and hepatic metabolomes in rats. Rats received daily intragastric administration of either CGA (60 mg/kg body weight) or distilled water (control) for 4 weeks. Growth performance, serum biochemical profiles, and hepatic morphology were measured. Additionally, serum and liver tissue extracts were analyzed for metabolomes by high-resolution 1H nuclear magnetic resonance-based metabolomics and multivariate statistics. CGA did not affect rat growth performance, serum biochemical profiles, or hepatic morphology. However, supplementation with CGA decreased serum concentrations of lactate, pyruvate, succinate, citrate, β-hydroxybutyrate and acetoacetate, while increasing serum concentrations of glycine and hepatic concentrations of glutathione. These results suggest that CGA supplementation results in perturbation of energy and amino acid metabolism in rats. We suggest that glycine and glutathione in serum may be useful biomarkers for biological properties of CGA on nitrogen metabolism in vivo.

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“…The DNA, RNA, and protein were extracted from the liver using the TRI Reagent-RNA/DNA/protein isolation reagent (Hou et al 2012;Wang et al 2013). Liver DNA was analyzed fluorimetrically using the method of Prasad et al (1972).…”

Section: Measurement Of Liver Dna Rna and Proteinmentioning

confidence: 99%

Dietary supplementation with glutamate precursor α-ketoglutarate attenuates lipopolysaccharide-induced liver injury in young pigs

Wang

Hou

et al. 2015

Amino Acids

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There is growing interest in glutamate as a functional amino acid in nutrition and health. This study was conducted to determine whether glutamate precursor α-ketoglutarate (AKG) could alleviate lipopolysaccharide (LPS)-induced liver injury in young pigs. Twenty-four piglets were randomly assigned to the control, LPS, or LPS + AKG group. Piglets in the control and LPS groups were fed a basal diet, whereas piglets in the NAC group were fed the basal diet supplemented with 1 % AKG. On days 10, 12, 14, and 16 of the trial, piglets in the LPS and LPS + AKG groups received intraperitoneal administration of LPS (80 μg/kg BW), whereas piglets in the control group received the same volume of saline. On day 16 of the trial, blood samples were collected 3 h after LPS or saline injection. Twenty-four hours post-administration of LPS or saline (on day 17 of the trial), piglets were killed to obtain liver for analysis. Dietary AKG supplementation alleviated LPS-induced histomorphological abnormalities and mitigated LPS-induced increases in aspartate aminotransferase (AST) activity and AST/ALT ratio (P < 0.05). Compared with the LPS group, dietary supplementation with AKG decreased plasma glutamate concentration, while increasing hepatic concentrations of glutamate, glutamine, leucine, asparagine, lysine, alanine, serine, threonine, valine, and phenylalanine (P < 0.05). LPS challenge dramatically increased concentrations of malondialdehyde and decreased glutathione peroxidase activity in the liver. Additionally, LPS challenge enhanced concentrations of AMP and total protein, as well as RNA/DNA and total protein/DNA ratios, while decreasing hepatic ADP concentrations. These adverse effects of LPS challenge were ameliorated by AKG supplementation. Collectively, dietary AKG supplementation provides a new means to ameliorate LPS-induced liver injury by increasing anti-oxidative capacity and improving energy metabolism in young pigs.

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

Cited by 58 publications

References 66 publications

N-acetylcysteine stimulates protein synthesis in enterocytes independently of glutathione synthesis

N-acetylcysteine stimulates protein synthesis in enterocytes independently of glutathione synthesis

Metabolomic analysis of amino acid and energy metabolism in rats supplemented with chlorogenic acid

Dietary supplementation with glutamate precursor α-ketoglutarate attenuates lipopolysaccharide-induced liver injury in young pigs

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