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Resveratrol Ameliorates Intestinal Damage Challenged With Deoxynivalenol Through Mitophagy in vitro and in vivo.

ABSTRACT: Deoxynivalenol (DON) reduces growth performance and damage intestinal function, and resveratrol (RES) has positive effects on growth performance and intestinal function. The purpose of this study was to investigate the protective mechanism of RES in vitro and vivo challenged with DON. The results showed that dietary supplementation with DON significantly increase the mRNA expression levels of mitophagy- related genes, and protein level for PINK1, Parkin, Beclin-1, Lamp, Atg5, Map1lc, Bnip3, Fundc1, Bcl2l1 and SQSTMS1 (P < 0.05), while supplementation with both RES and DON decreased those indexes in the ileum. Besides DON significantly decreased protein level for Pyruvate Dehydrogenase, Cytochrome c, MFN1, OPA1, and PHB1 (P < 0.05), while supplementation with both RES and DON increased protein level for PHB1, SDHA, and VDAC in the ileum. Moreover, in vitro, we found that DON significantly decreased mitochondrial respiration (P < 0.05), while RES + DON increased the rate of spare respiratory capacity. Also, DON significantly decreased total NAD and ATP (P < 0.05), while RES + DON increased the total NAD and ATP. These results indicate that RES may ameliorates the intestinal damage challenged with deoxynivalenol through mitophagy in weaning piglets.

SUBMITTER: Huang Y

PROVIDER: S-EPMC8793063 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Resveratrol Ameliorates Intestinal Damage Challenged With Deoxynivalenol Through Mitophagy in vitro and in vivo.

Huang Yujian Y Zheng Changbing C Song Bo B Wang Li L Xiao Hao H Jiang Zongyong Z

Frontiers in veterinary science 20220113

Deoxynivalenol (DON) reduces growth performance and damage intestinal function, and resveratrol (RES) has positive effects on growth performance and intestinal function. The purpose of this study was to investigate the protective mechanism of RES in vitro and vivo challenged with DON. The results showed that dietary supplementation with DON significantly increase the mRNA expression levels of mitophagy- related genes, and protein level for PINK1, Parkin, Beclin-1, Lamp, Atg5, Map1l ...[more]

PMID: 35097052

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Project description:BackgroundDeoxynivalenol (DON) is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals. Resveratrol (RES) effectively exerts anti-inflammatory and antioxidant effects. However, the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear. Therefore, this study aimed to investigate the effect of RES on growth performance, gut health and the gut microbiota in DON-challenged piglets. A total of 64 weaned piglets [Duroc × (Landrace × Yorkshire), 21-d-old, 6.97 ± 0.10 kg body weight (BW)] were randomly allocated to 4 treatment groups (8 replicate pens per treatment, each pen containing 2 males; n = 16 per treatment) for 28 d. The piglets were fed a control diet (CON) or the CON diet supplemented with 300 mg RES/kg diet (RES group), 3.8 mg DON/kg diet (DON) or both (DON+RES) in a 2 × 2 factorial design.ResultsDON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) mRNA and protein expression, and increased zonula occludens-1 (ZO-1) mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet (P < 0.05). Compared with unsupplemented DON-challenged piglets, infected piglets fed a diet with RES showed significantly decreased malondialdehyde (MDA) levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes (i.e., GCLC, GCLM, HO-1, SOD1 and NQO-1) and glutamate-cysteine-ligase modulatory subunit (GCLM) protein expression (P < 0.05). Moreover, RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets (P < 0.05). Finally, RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations, while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone (P < 0.05).ConclusionsRES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function, alleviating intestinal inflammation and oxidative damage, and positively modulating the gut microbiota. The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations, and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.

Project description:Sodium butyrate has gained increasing attention for its vast beneficial effects. However, whether sodium butyrate could alleviate oxidative stress-induced intestinal dysfunction and mitochondrial damage of piglets and its underlying mechanism remains unclear. The present study used a hydrogen peroxide- (H2O2-) induced oxidative stress model to study whether sodium butyrate could alleviate oxidative stress, intestinal epithelium injury, and mitochondrial dysfunction of porcine intestinal epithelial cells (IPEC-J2) in AMPK-mitophagy-dependent pathway. The results indicated that sodium butyrate alleviated the H2O2-induced oxidative stress, decreased the level of reactive oxygen species (ROS), increased mitochondrial membrane potential (MMP), mitochondrial DNA (mtDNA), and mRNA expression of genes related to mitochondrial function, and inhibited the release of mitochondrial cytochrome c (Cyt c). Sodium butyrate reduced the protein expression of recombinant NLR family, pyrin domain-containing protein 3 (NLRP3) and fluorescein isothiocyanate dextran 4 kDa (FD4) permeability and increased transepithelial resistance (TER) and the protein expression of tight junction. Sodium butyrate increased the expression of light-chain-associated protein B (LC3B) and Beclin-1, reduced the expression of P62, and enhanced mitophagy. However, the use of AMPK inhibitor or mitophagy inhibitor weakened the protective effect of sodium butyrate on mitochondrial function and intestinal epithelium barrier function and suppressed the induction effect of sodium butyrate on mitophagy. In addition, we also found that after interference with AMPKα, the protective effect of sodium butyrate on IPEC-J2 cells treated with H2O2 was suppressed, indicating that AMPKα is necessary for sodium butyrate to exert its protective effect. In summary, these results revealed that sodium butyrate induced mitophagy by activating AMPK, thereby alleviating oxidative stress, intestinal epithelium barrier injury, and mitochondrial dysfunction induced by H2O2.

Dataset Information

Resveratrol Ameliorates Intestinal Damage Challenged With Deoxynivalenol Through Mitophagy in vitro and in vivo.

Publications

Resveratrol Ameliorates Intestinal Damage Challenged With Deoxynivalenol Through Mitophagy <i>in vitro</i> and <i>in vivo</i>.

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