Effects of Dietary Supplementation with Glutamate and Aspartate on Diquat-Induced Oxidative Stress in Piglets

Yin, Jie; Liu, Mingfeng; Ren, Wenkai; Duan, Jielin; Yang, Guan; Zhao, Yurong; Fang, Rejun; Chen, Lixiang; Li, Tiejun; Yin, Yulong

doi:10.1371/journal.pone.0122893

Cited by 134 publications

(136 citation statements)

References 36 publications

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“…Intragastric or intraperitoneal administration of H 2 O 2 could decrease growth performance and caused oxidative stress [21–23]. Furthermore, previous studies showed that addition of H 2 O 2 (300 μ M) to chicken intestinal epithelial cells for 24 h significantly decreased cell survival and SOD activity [24].…”

Section: Discussionmentioning

confidence: 99%

N-Acetyl-L-cysteine Protects the Enterocyte against Oxidative Damage by Modulation of Mitochondrial Function

Xiao

Shao

et al. 2016

Mediators of Inflammation

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The neonatal small intestine is susceptible to damage caused by oxidative stress. This study aimed to evaluate the protective role of antioxidant N-acetylcysteine (NAC) in intestinal epithelial cells against oxidative damage induced by H2O2. IPEC-J2 cells were cultured in DMEM-H with NAC and H2O2. After 2-day incubation, IPEC-J2 cells were collected for analysis of DNA synthesis, antioxidation capacity, mitochondrial respiration, and cell apoptosis. The results showed that H2O2 significantly decreased (P < 0.05) proliferation rate, mitochondrial respiration, and antioxidation capacity and increased cell apoptosis and the abundance of associated proteins, including cytochrome C, Bcl-XL, cleaved caspase-3, and total caspase-3. NAC supplementation remarkably increased (P < 0.05) proliferation rate, antioxidation capacity, and mitochondrial bioenergetics but decreased cell apoptosis. These findings indicate that NAC might rescue the intestinal injury induced by H2O2.

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Section: Discussionmentioning

confidence: 99%

N-Acetyl-L-cysteine Protects the Enterocyte against Oxidative Damage by Modulation of Mitochondrial Function

Xiao

Shao

et al. 2016

Mediators of Inflammation

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“…Dexamethasone-suppressed protein synthesis is alleviated by leucine Growing evidence suggests that dietary supplementation with AA confers beneficial effects on stress (Yin et al, 2015). As an essential BCAA, the metabolic roles for L-leucine go far beyond serving exclusively as a substrate for de novo protein synthesis.…”

Section: Mtor Inhibition May Be Involved In Dexamethasonesuppressed Pmentioning

confidence: 99%

Glucocorticoids retard skeletal muscle development and myoblast protein synthesis through a mechanistic target of rapamycin (mTOR)-signaling pathway in broilers (Gallus gallus domesticus)

Wang

Jia

Xiao

et al. 2015

Stress

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Glucocorticoids exert a well-known catabolic protein action on skeletal muscle. The mechanistic target of rapamycin (mTOR) signaling pathway acts as a central regulator of protein metabolism. Whether glucocorticoids regulate protein synthesis through the mTOR pathway in skeletal muscle of chickens remains unknown. This study was performed to characterize the effect of glucocorticoids on the mTOR pathway in skeletal muscle development in chickens, and on protein synthesis in cultured embryonic myoblasts. Male 29-d-old chickens were given a dexamethasone injection (2 mg/kg) twice per day for 4 d (n = 16). Chicken embryonic myoblasts were exposed to dexamethasone for 24 h (100 µmol/L, n = 4 cultures). The interaction between dexamethasone and leucine was also investigated. ANOVA and Duncan's multiple test were used to analyze the effects of the dexamethasone and leucine treatments. The results showed that dexamethasone decreased body weight gain, body weight, and feed efficiency. Protein synthesis was inhibited by in vitro dexamethasone exposure. Phosphorylation of mTOR and ribosomal protein S6 protein kinase (p70S6K) were inhibited by dexamethasone, suggesting the mTOR pathway may be involved in dexamethasone-regulated muscle protein synthesis. Phosphorylation of AMP-activated protein kinase (AMPK) was not altered in vitro but was reduced in vivo by dexamethasone. These results imply that the mTOR and AMPK pathways are both involved in retarding muscle development and protein synthesis by glucocorticoids, but the mTOR pathway is a critical point linking glucocorticoid and protein synthesis. Leucine, at least partially, inhibited the effects of dexamethasone on protein synthesis via the mTOR pathway.

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“…This mucosal barrier function is impaired under conditions of oxidative stress brought about by excess reactive oxygen species (24). Diquat is widely used as an oxidant in in vitro or in vivo experiments to induce oxidative stress and apoptosis (25,26). Glutamate supplementation ameliorates endotoxin-induced damage to the jejunal epithelium and intestinal paracellular hyperpermeability (27,28), suggesting a critical role for Glu in intestinal-mucosal barrier function.…”

Section: Introductionmentioning

confidence: 99%

L-Glutamate Enhances Barrier and Antioxidative Functions in Intestinal Porcine Epithelial Cells,

Jiao

et al. 2015

The Journal of Nutrition

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Effects of Dietary Supplementation with Glutamate and Aspartate on Diquat-Induced Oxidative Stress in Piglets

Cited by 134 publications

References 36 publications

N-Acetyl-L-cysteine Protects the Enterocyte against Oxidative Damage by Modulation of Mitochondrial Function

N-Acetyl-L-cysteine Protects the Enterocyte against Oxidative Damage by Modulation of Mitochondrial Function

Glucocorticoids retard skeletal muscle development and myoblast protein synthesis through a mechanistic target of rapamycin (mTOR)-signaling pathway in broilers (Gallus gallus domesticus)

L-Glutamate Enhances Barrier and Antioxidative Functions in Intestinal Porcine Epithelial Cells,

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