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.

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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.

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Significant embryo loss remains a serious problem in pig production. Reactive oxygen species (ROS) play a critical role in embryonic implantation and placentation. However, the potential mechanism of ROS on porcine trophectoderm (pTr) cell fate during the peri-implantation period has not been investigated. This study aimed to elucidate the effects of ROS on pTr cell phenotypes and the regulatory role in cell attachment and differentiation. Herein, results showed that exogenous H2O2 inhibited pTr cell viability, arrested the cell cycle at S and G2/M phases, and increased cell apoptosis and autophagy protein light chain 3B and Beclin-1, whereas these effects were reversed by different concentrations of N-acetyl-l-cysteine (NAC) posttreatment. In addition, NAC abolished H2O2-induced autophagic flux, inhibited intracellular and mitochondrial ROS, and restored expression of genes important for mitochondrial DNA and biogenesis, cell attachment, and differentiation. NAC reversed H2O2-activated MAPK and Akt/mammalian target of rapamycin pathways in dose-dependent manners. Furthermore, analyses with pharmacological and RNA interference approaches suggested that autophagy regulated cell apoptosis and gene expression of caudal-related homeobox 2 and IL-1β. Collectively, these results provide new insights into the role of the ROS-induced autophagy in pTr cell apoptosis, attachment, and differentiation, indicating a promising target for decreasing porcine conceptus loss during the peri-implantation period.

This study investigated the effects of weaning on the hepatic redox status, apoptosis, function, and the mitogen-activated protein kinase (MAPK) signaling pathways during the first week after weaning in piglets. A total of 12 litters of piglets were weaned at d 21 and divided into the weaning group (WG) and the control group (CG). Six piglets from each group were slaughtered at d 0 (d 20, referred to weaning), d 1, d 4, and d 7 after weaning. Results showed that weaning significantly increased the concentrations of hepatic free radicals H2O2 and NO, malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG), while significantly decreasing the inhibitory hydroxyl ability (IHA) and glutathione peroxidase (GSH-Px), and altered the level of superoxide dismutase (SOD). The apoptosis results showed that weaning increased the concentrations of caspase-3, caspase-8, caspase-9 and the ratio of Bax/Bcl-2. In addition, aspartate aminotransferase transaminase (AST) and alanine aminotransferase (ALT) in liver homogenates increased after weaning. The phosphorylated JNK and ERK1/2 increased, while the activated p38 initially decreased and then increased. Our results suggested that weaning increased the hepatic oxidative stress and aminotransferases and initiated apoptosis, which may be related to the activated MAPK pathways in postweaning piglets.

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