Dimethylglycine sodium salt activates Nrf2/SIRT1/PGC1α leading to the recovery of muscle stem cell dysfunction in newborns with intrauterine growth restriction.

The objectives of this study were focused on the mechanism of mitochondrial dysfunction in skeletal muscle stem cells (MuSCs) from intrauterine growth restriction (IUGR) newborn piglets, and the relief of dimethylglycine sodium salt (DMG-Na) on MuSCs mitochondrial dysfunction by Nrf2/SIRT1/PGC1α network. In this study, six newborn piglets with normal birth weight (NBW) and six IUGR newborn piglets were slaughtered immediately after birth to obtain longissimus dorsi muscle (LM) samples. MuSCs were collected and divided into three groups: MuSCs from NBW newborn piglets (N), MuSCs from IUGR newborn piglets (I), and MuSCs from IUGR newborn piglets with 32 µmol DMG-Na (ID). Compared with the NBW group, the IUGR group showed decreased (P < 0.05) serum and LM antioxidant defense capacity, and increased (P < 0.05) serum and LM damage. Compared with the N group, the I group showed decreased (P < 0.05) MuSCs antioxidant defense capacity, mitochondrial ETC complexes, energy metabolites, and antioxidant defense-related and mitochondrial function-related gene and protein expression levels. The antioxidant defense capacity, mitochondrial ETC complexes, energy metabolites, and antioxidant defense-related and mitochondrial function-related gene and protein expression levels of MuSCs were improved (P < 0.05) in the ID group compared to those in the I group. The MuSCs of IUGR newborns activate the Nrf2/SIRT1/PGC1α network by taking in DMG-Na, thereby neutralizing excessive generated O2•- that may help to improve their unfavorable mitochondrial dysfunction in skeletal muscle.

Dietary taurine supplementation attenuates lipopolysaccharide-induced inflammatory responses and oxidative stress of broiler chickens at an early age.

This study was conducted to investigate the effect of taurine as a prophylactic treatment on antioxidant function and inflammatory responses of broilers challenged with lipopolysaccharide (LPS). A total of 256 one-day-old male Arbor Acres broiler chicks were randomly assigned to four treatments with eight replicates of eight birds (eight birds per cage). Four treatment groups were designated as follows: 1) in the CON group, broilers fed a basal diet; 2) in the LPS group, LPS-challenged broilers fed a basal diet; 3) in the LPS + T1 group, LPS-challenged broilers fed a basal diet supplemented with 5.0 g/kg taurine; and 4) in the LPS + T2 group, LPS-challenged broilers fed a basal diet supplemented with 7.5 g/kg taurine. The LPS-challenged broilers were intraperitoneally injected with 1 mg/kg body weight (BW) of LPS at 16, 18, and 20 d of age, whereas the CON group received an injection of sterile saline. The results showed that broilers injected with LPS exhibited decreased (P < 0.05) the average daily gain (ADG) and the 21-d BW (P < 0.05), while taurine supplementation alleviated the negative effects of LPS. Additionally, the LPS-induced increases (P < 0.05) in serum alanine transaminase and aspartate transaminase activities were reversed by taurine supplementation. The taurines could alleviate the hepatic oxidative stress, with the presence of lower content of malondialdehyde (P < 0.05), higher content of glutathione (P < 0.05), and an increased glutathione peroxidase (GSH-Px) activity (P < 0.05). The concentrations of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the liver were measured by ELISA kits, and the result showed that dietary taurine supplementation prevented these cytokines increases in the liver of LPS-induced broilers. Taurine reduced the genes expression of IL-1ß, TNF-α, IL-6, cyclooxygenase-2, and inducible nitric oxide synthase, whereas it boosted the expression levels of antioxidant-related genes (nuclear factor erythroid 2-related factor 2, heme oxygenase-1, glutamate-cysteine ligase catalytic subunit, and GSH-Px) in the liver of LPS-induced broilers. In conclusion, dietary taurine supplementation in broilers mitigated LPS-induced defects in ADG, oxidative stress, and inflammatory responses.

Curcumin Alleviates IUGR Jejunum Damage by Increasing Antioxidant Capacity through Nrf2/Keap1 Pathway in Growing Pigs.

The purpose of this study was to explore the effects of curcumin on IUGR jejunum damage. A total of 24 IUGR and 12 normal-birth weight (NBW) female crossbred (Duroc × Landrace × Large White) piglets were randomly assigned into three groups at weaning (26 days): IUGR group, NBW group, and IUGR + CUR group, which were fed diets containing 0 mg/kg (NBW), 0 mg/kg (IUGR) and 200 mg/kg (IUGR + CUR) curcumin from 26 to 115 days of age. Results showed that dietary supplementation with 200 mg/kg curcumin significantly increased the total superoxide dismutase (T-SOD) activity and decreased the malondialdehyde (MDA) content in the jejunum of IUGR pigs (p < 0.05). Results of real-time PCR showed that the IUGR + CUR group significantly increased the gene expression of NF-E2-related factor 2 (Nrf2) (p < 0.05), and increased the glutamate-cysteine ligase catalytic subunit (GCLC), superoxide dismutase 1 (SOD1), glutamate-cysteine ligase modifier subunit (GCLM), and NAD(P)H quinone dehydrogenase 1 (NQO1) mRNA expression compared with the IUGR group (p < 0.05). Western blot results showed that dietary supplementation with 200 mg/kg curcumin significantly increased the protein levels of Nrf2 and NQO1. Compared with the IUGR group, pigs in IUGR + CUR group showed significantly decreased the levels of tumor necrosis factor-α (TNFα), interleukin-6 (IL-6), and interferon gamma (IFNγ) (p < 0.05), and increased the interleukin-2 (IL-2) level (p < 0.05). Dietary supplementation with 200 mg/kg curcumin significantly reduced cysteinyl aspartate specific proteinase 3 (caspase3), BCL2-associated X protein (bax), B-cellCLL/lymphoma 2 (bcl2), and heat-shock protein 70 (hsp70) mRNA expression, and increased occludin (ocln) mRNA expression (p < 0.05). In conclusion, dietary supplementation with 200 mg/kg curcumin can alleviate jejunum damage in IUGR growing pigs, through Nrf2/Keap1 pathway.