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- Title
Glutathione Protects against Paraquat-Induced Oxidative Stress by Regulating Intestinal Barrier, Antioxidant Capacity, and CAR Signaling Pathway in Weaned Piglets.
- Authors
Xiang, Xuan; Wang, Houfu; Zhou, Wentao; Wang, Chenyu; Guan, Peng; Xu, Gang; Zhao, Qiang; He, Liuqin; Yin, Yulong; Li, Tiejun
- Abstract
Endogenous glutathione (GSH) effectively regulates redox homeostasis in the body. This study aimed to investigate the regulatory mechanism of different dietary levels of GSH supplementation on the intestinal barrier and antioxidant function in a paraquat-induced stress-weaned piglet model. Our results showed that dietary 0.06% GSH supplementation improved the growth performance of weaned piglets under normal and stressful conditions to some degree and decreased the diarrhea rate throughout. Exogenous GSH improved paraquat-induced changes in intestinal morphology, organelle, and permeability and reduced intestinal epithelial cell apoptosis. Moreover, GSH treatment alleviated intestinal oxidative stress damage by upregulating antioxidant (GPX4, CnZnSOD, GCLC, and GCLM) and anti-inflammatory (IL-10) gene expression and downregulating inflammatory cytokines (IFN-γ and IL-12) gene expression. Furthermore, GSH significantly reduced the expression levels of constitutive androstane receptor (CAR), RXRα, HSP90, PP2Ac, CYP2B22, and CYP3A29, and increased the expression levels of GSTA1 and GSTA2 in the jejunum and ileum of paraquat-induced piglets. We conclude that exogenous GSH protects against oxidative stress damage by regulating the intestinal barrier, antioxidant capacity, and CAR signaling pathway.
- Subjects
ANTIOXIDANT analysis; GLUTATHIONE; HOMEOSTASIS; HUMAN growth; REVERSE transcriptase polymerase chain reaction; CYTOKINES; INTERLEUKINS; DIARRHEA; ANIMAL experimentation; IMMUNOHISTOCHEMISTRY; ONE-way analysis of variance; SWINE; APOPTOSIS; OXIDATIVE stress; CELLULAR signal transduction; DIETARY supplements; ELECTRON microscopy; DESCRIPTIVE statistics; GENE expression profiling; MESSENGER RNA; RESEARCH funding; DATA analysis software
- Publication
Nutrients, 2023, Vol 15, Issue 1, p198
- ISSN
2072-6643
- Publication type
Article
- DOI
10.3390/nu15010198