The objective of this experiment was to investigate the influence of weaning stress and an antioxidant blend on gut health and free radical metabolism in postweaning pigs. A total of 96 pigs from 12 litters were randomly divided by litter to 3 groups with 4 litters each. The control group and the weaning group were fed the basal diet, and the antioxidant group was fed the basal diet supplemented with an antioxidant blend. The control group was suckling normally during the experimental period and the other 2 treatments were weaned at 21 d of age. Morphology in different parts of the intestines was used as a measure of intestinal barrier function. Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the concentrations of malondialdehyde (MDA), NO, H(2)O(2), and O(2) were measured in serum. Activities of the digestive enzymes, including sucrase, maltase, amylase, lipase, and pepsin, were measured at 24 d of age for all treatments. Gene expressions of free radicals, digestive enzymes, or antioxidant enzymes were selected for quantitative reverse transcription-PCR analyses. Results showed that weaning resulted in reductions (P< 0.05) in the villus height and width, and activity of digestive enzymes. Activity of SOD decreased (P < 0.05) and the concentrations of MDA, NO, and H(2)O(2) increased (P < 0.05) after weaning. The expression results indicated that the genes related to the antioxidant enzymes and digestive enzymes were down regulated (P < 0.05) after weaning. Tumor protein 53, which regulates reactive oxygen-species generation, tended to increase (P < 0.10) in the weaning group. The concentration of PPARγ coactivator-1α (PGC-1α), which plays an important protective role against oxidative stress by regulating the expression of mitochondrial antioxidants, was reduced (P < 0.05) in weaning pigs and increased (P < 0.01) in antioxidant pigs compared with the control pigs. Results indicated that intestinal dysfunction occurred after weaning and there was an inhibition of the antioxidant system. The antioxidant blend has the potential to prevent free radical-induced damage and suppress oxidative stress by modulating the expressions of tumor protein 53 and PGC-1α genes.

The objective of this experiment was to investigate the influence of weaning stress and an antioxidant blend on gut health and free radical metabolism in postweaning pigs. A total of 96 pigs from 12 litters were randomly divided by litter to 3 groups with 4 litters each. The control group and the weaning group were fed the basal diet, and the antioxidant group was fed the basal diet supplemented with an antioxidant blend. The control group was suckling normally during the experimental period and the other 2 treatments were weaned at 21 d of age. Morphology in different parts of the intestines was used as a measure of intestinal barrier function. Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the concentrations of malondialdehyde (MDA), NO, H(2)O(2), and O(2) were measured in serum. Activities of the digestive enzymes, including sucrase, maltase, amylase, lipase, and pepsin, were measured at 24 d of age for all treatments. Gene expressions of free radicals, digestive enzymes, or antioxidant enzymes were selected for quantitative reverse transcription-PCR analyses. Results showed that weaning resulted in reductions (P< 0.05) in the villus height and width, and activity of digestive enzymes. Activity of SOD decreased (P < 0.05) and the concentrations of MDA, NO, and H(2)O(2) increased (P < 0.05) after weaning. The expression results indicated that the genes related to the antioxidant enzymes and digestive enzymes were down regulated (P < 0.05) after weaning. Tumor protein 53, which regulates reactive oxygen-species generation, tended to increase (P < 0.10) in the weaning group. The concentration of PPARγ coactivator-1α (PGC-1α), which plays an important protective role against oxidative stress by regulating the expression of mitochondrial antioxidants, was reduced (P < 0.05) in weaning pigs and increased (P < 0.01) in antioxidant pigs compared with the control pigs. Results indicated that intestinal dysfunction occurred after weaning and there was an inhibition of the antioxidant system. The antioxidant blend has the potential to prevent free radical-induced damage and suppress oxidative stress by modulating the expressions of tumor protein 53 and PGC-1α genes.

In this study, antioxidant capability and protective effect of probiotics on reproductive damage induced by diet oxidative stress were investigated. Thirty male Sprague-Dawley rats were randomly divided into three groups with 10 rats in each group. The control group consumed a normal standard diet (5% fat, w/w). The other two treatment groups were fed with a high-fat diet (20% fat, w/w), and a high-fat diet supplemented with 2% probiotics (w/w), respectively. At the end of the experimental period, that is, after 6 weeks, rats were killed. Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), contents of nitric oxide (NO) free radical and malondialdehyde (MDA) in serum and sperm suspension were examined. Sperm parameters including sperm concentration, viability, motility and DNA integrity were analyzed. The results showed that high-fat diet could induce oxidative stress, shown as significant increases in lipid peroxidation, NO free radical, significant decrease in activities of SOD, GSH-Px, significant reduction in sperm concentration, viability and motility, and damage in sperm DNA ( P , 0.05), compared with the control group. These alterations were significantly reversed in the probiotics-supplemented group and had no significant difference in antioxidant capability, lipid peroxidation and sperm parameters compared with the control group. The percentage of sperm with DNA damage was significantly lower than the high-fat diet group and still higher than the control group, which means that probiotics could attenuate sperm damage to some extent. The present results indicated that dietary probiotics had antioxidant activity and the protective effect against sperm damage induced by high-fat diet to some extent.

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.