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Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway
BACKGROUND: Necrotizing enterocolitis (NEC) is often associated with exaggerated activation of inflammatory response. Astaxanthin has been shown in studies to have a positive and advantageous effect on anti-inflammatory response. Hence, it is of great significance to study the protective effect of a...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10070044/ https://www.ncbi.nlm.nih.gov/pubmed/37021078 http://dx.doi.org/10.1155/2023/6078308 |
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author | Zhang, Xuandong Luo, Yujia Gu, Rui Jiang, Zhou |
author_facet | Zhang, Xuandong Luo, Yujia Gu, Rui Jiang, Zhou |
author_sort | Zhang, Xuandong |
collection | PubMed |
description | BACKGROUND: Necrotizing enterocolitis (NEC) is often associated with exaggerated activation of inflammatory response. Astaxanthin has been shown in studies to have a positive and advantageous effect on anti-inflammatory response. Hence, it is of great significance to study the protective effect of astaxanthin in NEC disease and its molecular mechanism. OBJECTIVE: The present study was to investigate whether astaxanthin attenuates NEC rats and to explore its potential mechanism. Material and Methods. Hematoxylin-eosin staining was used to observe the pathological change of the intestinal tissue in NEC rats. Subsequently, we determined the anti-oxidative stress, anti-apoptosis, and anti-inflammation in astaxanthin with enzyme-linked immunosorbent assay kits, TUNEL staining, western blot, and immunohistochemistry assay. Furthermore, we added nucleotide-binding oligomerization domain 2 (NOD2) inhibitor to certify the molecular pathway of the astaxanthin in NEC rats. RESULTS: Astaxanthin improved the pathological changes of the intestinal tissues. It restrained inflammation, oxidative stress, and protected cells from apoptosis in the intestinal tissue and serum of the NEC rats. Moreover, astaxanthin enhanced NOD2, whereas it suppressed toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB) pathway-related proteins. Apart from that, the NOD2 inhibitor offset the protective effect of the astaxanthin towards the NEC rats. CONCLUSION: The present study indicated that astaxanthin alleviated oxidative stress, inflammatory response, and apoptosis in NEC rats by enhancing NOD2 and inhibiting TLR4 pathway. |
format | Online Article Text |
id | pubmed-10070044 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-100700442023-04-04 Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway Zhang, Xuandong Luo, Yujia Gu, Rui Jiang, Zhou Gastroenterol Res Pract Research Article BACKGROUND: Necrotizing enterocolitis (NEC) is often associated with exaggerated activation of inflammatory response. Astaxanthin has been shown in studies to have a positive and advantageous effect on anti-inflammatory response. Hence, it is of great significance to study the protective effect of astaxanthin in NEC disease and its molecular mechanism. OBJECTIVE: The present study was to investigate whether astaxanthin attenuates NEC rats and to explore its potential mechanism. Material and Methods. Hematoxylin-eosin staining was used to observe the pathological change of the intestinal tissue in NEC rats. Subsequently, we determined the anti-oxidative stress, anti-apoptosis, and anti-inflammation in astaxanthin with enzyme-linked immunosorbent assay kits, TUNEL staining, western blot, and immunohistochemistry assay. Furthermore, we added nucleotide-binding oligomerization domain 2 (NOD2) inhibitor to certify the molecular pathway of the astaxanthin in NEC rats. RESULTS: Astaxanthin improved the pathological changes of the intestinal tissues. It restrained inflammation, oxidative stress, and protected cells from apoptosis in the intestinal tissue and serum of the NEC rats. Moreover, astaxanthin enhanced NOD2, whereas it suppressed toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB) pathway-related proteins. Apart from that, the NOD2 inhibitor offset the protective effect of the astaxanthin towards the NEC rats. CONCLUSION: The present study indicated that astaxanthin alleviated oxidative stress, inflammatory response, and apoptosis in NEC rats by enhancing NOD2 and inhibiting TLR4 pathway. Hindawi 2023-03-27 /pmc/articles/PMC10070044/ /pubmed/37021078 http://dx.doi.org/10.1155/2023/6078308 Text en Copyright © 2023 Xuandong Zhang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhang, Xuandong Luo, Yujia Gu, Rui Jiang, Zhou Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway |
title | Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway |
title_full | Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway |
title_fullStr | Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway |
title_full_unstemmed | Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway |
title_short | Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway |
title_sort | astaxanthin alleviates inflammatory response in neonatal necrotizing enterocolitis rats by regulating nod2/tlr4 pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10070044/ https://www.ncbi.nlm.nih.gov/pubmed/37021078 http://dx.doi.org/10.1155/2023/6078308 |
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