Glutamine protects cow's ruminal epithelial cells from acid-induced injury in vitro

<br />This study was conducted to investigate the effects and mechanisms of glutamine (Gln) on the repair of acid-induced injury in dairy cow ruminal epithelial cells (RECs) <i>in vitro</i>. Dairy cow RECs were cultured in a medium with pH of 5.5 for 3 h and subsequently treated with various concentrations of Gln (4, 8, 12, 32 mmol/l) for 12 h. The messenger ribonucleic acid (mRNA) expression levels of occludin (<i>OCLN</i>)<i>,</i> claudin 1 (<i>CLDN1</i>)<i>, </i>toll-like receptor 2 (<i>TLR2</i>)<i>, </i>toll-like receptor 4 (<i>TLR4</i>) and genes for inflammatory factors were measured using reverse transcription-quantitative real-time PCR (RT-qPCR). The results showed that cellular activity and <i>OCLN</i> expression were significantly highest at 8 mmol/l Gln (<i>P </i>< 0.05). <i>CLDN1</i> expression was significantly higher at 4 mmol/l Gln compared to the other groups (<i>P </i>< 0.05). The relative expression levels of tumour necrosis factor (<i>TNF</i>)<i>, </i>interleukin 1B (<i>IL1B</i>)<i>, </i>C-X-C motif chemokine ligand 8 (<i>CXCL8</i>), <i>TLR2</i> and <i>TLR4 </i>in the acid treatment group were significantly higher than those in the control group (<i>P </i>< 0.05), but they were lower in the Gln-treated groups than in the acid treatment group (<i>P </i>< 0.05). These findings demonstrate that Gln promotes the proliferation of RECs, enhances the expression of epithelial cell junction proteins, and inhibits the expression of inflammatory factors and surface receptors. In conclusion, Gln shows a potential for repairing acid-induced injury in RECs.

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Publication Details

Journal
Czech Journal of Animal Science
Published
2024-10-16
DOI
https://doi.org/10.17221/170/2023-cjas
Citations
2
Primary Topic
Ruminant Nutrition and Digestive Physiology
Type
article
Field-Weighted Citation Impact
1.14
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article

Glutamine protects cow's ruminal epithelial cells from acid-induced injury in vitro

Mengying Dou, Zihan Zhao, Feiyan Zhao, Zhijun Cao et al.
2 citations
Czech Journal of Animal Science
Ruminant Nutrition and Digestive Physiology
1.14
article

Glutamine protects cow's ruminal epithelial cells from acid-induced injury in vitro

Mengying Dou, Zihan Zhao, Feiyan Zhao, Zhijun Cao, Yan Yu, Ke Ding, Li Wang, Cai Zhang, Yuanxiao Li
article en
2 citations

Abstract

<br />This study was conducted to investigate the effects and mechanisms of glutamine (Gln) on the repair of acid-induced injury in dairy cow ruminal epithelial cells (RECs) <i>in vitro</i>. Dairy cow RECs were cultured in a medium with pH of 5.5 for 3 h and subsequently treated with various concentrations of Gln (4, 8, 12, 32 mmol/l) for 12 h. The messenger ribonucleic acid (mRNA) expression levels of occludin (<i>OCLN</i>)<i>,</i> claudin 1 (<i>CLDN1</i>)<i>, </i>toll-like receptor 2 (<i>TLR2</i>)<i>, </i>toll-like receptor 4 (<i>TLR4</i>) and genes for inflammatory factors were measured using reverse transcription-quantitative real-time PCR (RT-qPCR). The results showed that cellular activity and <i>OCLN</i> expression were significantly highest at 8 mmol/l Gln (<i>P </i>< 0.05). <i>CLDN1</i> expression was significantly higher at 4 mmol/l Gln compared to the other groups (<i>P </i>< 0.05). The relative expression levels of tumour necrosis factor (<i>TNF</i>)<i>, </i>interleukin 1B (<i>IL1B</i>)<i>, </i>C-X-C motif chemokine ligand 8 (<i>CXCL8</i>), <i>TLR2</i> and <i>TLR4 </i>in the acid treatment group were significantly higher than those in the control group (<i>P </i>< 0.05), but they were lower in the Gln-treated groups than in the acid treatment group (<i>P </i>< 0.05). These findings demonstrate that Gln promotes the proliferation of RECs, enhances the expression of epithelial cell junction proteins, and inhibits the expression of inflammatory factors and surface receptors. In conclusion, Gln shows a potential for repairing acid-induced injury in RECs.

Czech Journal of Animal ScienceVol. 69(10)
Zero hunger
Openalex Percentile: Top 20%
Ruminant Nutrition and Digestive Physiology
1.14
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