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.

The imbalance of redox biology and oxidative stress leads to intestinal barrier injury and mitophagy. However, much uncertainty still exists about the role of mitophagy in oxidative stress and intestinal function. Here, we showed the effects of hydrogen peroxide (H₂O₂)-induced oxidative stress on intestinal epithelial cell oxidation balance, intestinal barrier function and mitochondrial energy metabolism and its underlying mechanism. In this study, we found that H₂O₂-induced oxidative stress activated adenosine monophosphate-activated protein kinase (AMPK) and enhanced mitophagy in intestinal porcine epithelial cells (IPEC-J2). While compound C (AMPK inhibitor) and mdivi-1 (mitophagy inhibitor) significantly reduced the activity of superoxide dismutase (SOD) and increased mitochondrial reactive oxygen species (ROS) levels in H₂O₂ treated cells. Moreover, compound C and mdivi-1 significantly reduced the trans-epithelium electrical resistant (TER) and increased the fluorescein isothiocyanate-dextran (FD4) flux in H₂O₂ treated IPEC-J2. Furthermore, compound C and mdivi-1 significantly reduced the activity of mitochondrial complex II. Seahorse XF96 data showed that compound C + mdivi-1+ H₂O₂ treatment significantly reduced maximum respiratory oxygen consumption and spare respiratory capacity. Additionally, compound C or mdivi-1 treatment reduced the formation of mitochondrial autophagosomes. These results unveiled that AMPK and PINK1/Parkin mediated mitophagy is necessary for alleviating oxidative stress induced intestinal epithelial barrier damage and mitochondrial energy metabolism dysfunction in IPEC-J2.

Hesperidin alleviated mitochondrial calcium overload via inhibiting ER–mitochondrial calcium transfer mediated by IP3Rs in MAMs, which improved mitochondrial function and alleviated DON-induced oxidative stress and intestinal injury in piglets.

This study aimed to investigate the potential effects of resveratrol (RES) on intestinal function and oxidative stress in deoxynivalenol (DON)-challenged piglets. Twenty-four healthy Duroc × Yorkshire × Landrace weaned piglets at the age of 28 ± 1 days were randomly divided into four groups with six repetitions per group. The four groups were as follows: the control group (CON), fed with a basic diet; the RES group, fed with a basal diet + 300 mg/kg RES; the DON group, fed with a basal diet containing 2.65 mg/kg DON; and the DON + RES group, fed with a basal diet containing 2.65 mg/kg DON + 300 mg/kg RES. The results showed that the growth performance and intestinal function of DON-challenged piglets were significantly decreased (p < 0.05). Compared with the DON group, the average daily feed intake of piglets in the DON + RES group was significantly increased (p < 0.05). Additionally, dietary RES ameliorated DON-induced intestinal morphology impairment, as indicated by the increased (p < 0.05) jejunal villi height and the ratio of the jejunal villi height/crypt depth. Furthermore, after the addition of RES, the activities of superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) in the jejunum mucosa were significantly increased, and the content of malondialdehyde (MDA) was significantly declined (p < 0.05). In addition, the level of reactive oxygen species (ROS) in the mitochondria was significantly reduced by RES, while the mitochondrial membrane potential in jejunum was significantly increased by RES (p < 0.05). However, there was no obvious difference between DON + RES and DON groups on average daily gain and the ratio of feed togain, except for the significant inhibition of average daily feed intake (p < 0.05). In conclusion, RES could effectively alleviate the DON-induced oxidative stress on weaned piglets, and reduce the damage to mitochondria and intestinal morphology, so as to improve the growth performance of piglets.

This study aimed to investigate the effects of enzyme-bacteria co-fermented rapeseed meal (FRSM) on the growth performance, serum biochemical parameters, meat quality, and lipid metabolism of finishing pigs. A total of twenty-eight Duroc × Landrace × Yorkshire finishing pigs (4 months of age; initial body weight: 60.92 ± 1.08 kg) were randomly allotted to one of four dietary treatments for a 45-day feeding trial, consisting of corn-soybean meal diet (CSD) and three experimental diets in which 50, 75 and 100% of soybean meal in the corn-soybean diet was replaced with FRSM. Results showed that replacing soybean meal with FRSM had no negative effects on the growth performance of finishing pigs, maintaining average daily gain and feed efficiency (p > 0.05). Compared with the CSD group, the FRSM group exhibited lower serum cholesterol (p < 0.05). The serum low-density lipoprotein cholesterol, alanine aminotransferase, and urea content levels were lower in the FRSM75 or FRSM100 groups than in the CSD group (p < 0.05). Compared to the CSD, FRSM feeding increased the pH_24h and triglyceride content but significantly decreased the drip loss, shear force and chewiness in longissimus thoracis et lumborum (LTL) muscle (p < 0.05). Importantly, compared with the CSD, FRSM feeding significantly lowered the muscle SFA/UFA ratio, increased the PUFA/SFA ratio, and elevated threonine and valine levels (p < 0.05). The FRSM100 group exhibited further increases in umami amino acids (AAs), total essential AAs, and total AAs (p < 0.05). Morphological analysis indicated that, compared to CSD, the FRSM100 group had a significantly reduced muscle fiber perimeter in the LTL muscle (p < 0.05). Moreover, FRSM feeding up-regulated the expression levels of MyHC I and MyHC IIa and the lipogenic genes FASN, SREBP1, and SCD (p < 0.05). These results indicated that compared with rapeseed meal, FRSM exhibited a positive effect on improving the meat quality and lipid metabolism in finishing pigs and can be used as a suitable alternative protein source for soybean meal in finishing pig diets.