This study was conducted to explore the regulation of N-acetyl cysteine (NAC) on gut redox status and proliferation of selected microbiota in weaned piglets. A total of 150 newborn piglets from 15 litters were randomly divided by litter to the control group (normally suckling), the weaning group (fed the basal diet), and the NAC group (basal + NAC diet) with 5 litters per group. Activities of total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and inhibition capacity of hydroxyl radical (IHR), and contents of malondialdehyde (MDA), H2O2, and NO in the ileum, colon, and cecum were analyzed to profile oxidative stress states. The real-time absolute quantitative PCR reaction was employed to quantify the amounts of total bacteria, Lactobacillus, Bifidobacterium, and Escherichia coli. The N-acetyl cysteine, as a universal antioxidant, was used to improve the redox status. Results showed that weaning stress resulted in the occurrence of gut oxidative stress and changes of gut microbiota (P < 0.05). Compared with the weaned piglets, the activities of ileal, colonic, and cecal T-AOC; ileal and colonic GSH-Px; cecal SOD; and colonic and cecal IHR were enhanced (P < 0.05), and the concentrations of ileal and cecal H2O2, ileal and colonic NO, and colonic MDA were reduced (P < 0.05) in the NAC-treated piglets. An increase (P < 0.05) in gut Lactobacillus and Bifidobacterium, accompanied with a decrease (P < 0.05) in Escherichia coli counts, was also observed in the NAC group. Bivariate correlation indicated that Lactobacillus and Bifidobacterium were positively correlated (P < 0.05) with the activities of T-AOC, GSH-Px, and SOD and inversely related (P < 0.05) to increased levels of H2O2, NO, OH, and MDA, and Escherichia coli showed a strong positive association (P < 0.05) with increased levels of free radicals and MDA and a negative association (P < 0.05) with the activities of antioxidant enzymes in intestines of weaned piglets. We concluded that NAC constructively regulated on the changes of the gut redox status and microbiota in piglets in response to weaning stress. The observed correlations implied that the NAC effects on the gut microbiota were confirmed, partly through an effect on oxidative stress in piglets, providing evidence that gut microbiota may be potentially improved by the modulation of the redox status by an antioxidant, which has relevance for gut health and function.
In swine production, weaning is a critical event for porcine weaning-associated disease, such as postweaning stress syndrome, which involves intestinal dysfunction. However, little is known about the molecular mechanisms of intestinal dysfunction in pigs during weaning. To gain new insight into the interaction between weaning stress and intestinal function, 4 pigs at 25 d of age for each of the weaning and the suckling groups for a total of 40 pigs were used to analyze changes in the genomic expression in the intestines of weaned pigs by microarray analysis. Four hundred forty-five genes showed altered expression after weaning treatment (286 upregulated and 159 downregulated) at the cutoff criteria of the fold change ≥1.5 or <0.67 and P < 0.05. Most of these altered genes are cellular process related and regulators that may be involved in biological regulation, developmental processes, and metabolic processes. A keen interest was paid in deciphering expression changes in apoptosis or cell cycle control genes. The altered genomic expression of 8 selected genes related to the cell cycle process was confirmed by quantitative real-time PCR. Of the 8 genes tested, increased (P < 0.05) expression of genes involved in apoptosis (cytochrome c, somatic, and ataxia telangiectasia mutated), pro-inflammatory signals (tumor necrosis factor and NO synthases 2), and a transcription factor (nuclear factor of activated T cells, cytoplasmic, and calcineurin-dependent 2) were detected in weaned pigs compared with suckling pigs, but the expression of cell cycle control-related genes, such as E2F transcription factor 5-like, was lower (P < 0.05) in weaned pigs than suckling pigs. Weaned pigs also showed increased interleukin 8 expression and decreased SMAD family member 4 expression although no significant differences (P > 0.05) were observed when compared with the suckling pigs. These selected genes likely indicate that weaning induced cell cycle arrest, enhanced apoptosis, and inhibited cell proliferation. The results of this study provide a basis for understanding the molecular pathogenesis of weaning treatment.
Patient screening is important for early diagnosis of colorectal cancer (CRC). The present study aimed to compare the multitarget stool DNA (mt-sDNA) test with the fecal occult blood test (FOBT) for CRC screening. A total of 151 individuals were screened using colonoscopy, mt-sDNA and FOBT for the detection of CRC and adenoma. The results of the mt-sDNA test and FOBT were compared with colonoscopy to examine their sensitivity and specificity. Subsequently, the sensitivity and specificity of the mt-sDNA test were compared with those of FOBT in CRC and large adenoma. Stool samples were collected from patients with CRC (n=50) or large adenoma (n=51), as well as from normal controls (n=50). The mt-sDNA test outperformed FOBT in detecting CRC with a sensitivity of 90.0% (45/50) vs. 42.0% (21/50), advanced adenoma with a sensitivity of 70.6% (36/51) vs. 19.6% (10/51), stage I-III CRC with a sensitivity of 91.9% (34/37) vs. 29.7% (11/37), and stage IV CRC with a sensitivity of 84.6% (11/13) vs. 76.9% (10/13). In addition, the mt-sDNA test exhibited a specificity of 94.0% (47/50) in detecting CRC, which was superior to FOBT with a specificity of 90.0% (45/50). Therefore, the mt-sDNA test may have higher sensitivity and specificity compared with FOBT in diagnosing both CRC and advanced adenoma. KRAS mutations are detected in 30-40% of CRCs (1). There are seven mutation hotspots that account for >90% of the KRAS mutations, including Gly12Asp, Gly12Val, Gly12Ser, Gly12Cys, Gly12Ala, Gly12Arg and Gly13Asp (8). It has been demonstrated that mutations in codons 12 and 13 of exon 2 of KRAS are closely associated with the development of CRC, and mutations in codon 12 are associated with a less favorable prognosis compared with mutations in codon 13 (9).
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