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Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling
Myocardial ischemia/reperfusion (I/R) injury is marked by rapid increase in inflammation and not only results in myocardial apoptosis but also compromises the myocardial function. Dunaliella salina (D. salina), a halophilic unicellular microalga, has been used as a provitamin A carotenoid supplement...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9963554/ https://www.ncbi.nlm.nih.gov/pubmed/36835281 http://dx.doi.org/10.3390/ijms24043871 |
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author | Tsai, Chin-Feng Lin, Hui-Wen Liao, Jiuan-Miaw Chen, Ke-Min Tsai, Jen-Wei Chang, Chia-Sung Chou, Chia-Yu Su, Hsing-Hui Liu, Pei-Hsun Chu, Ya-Chun Wang, Yi-Hsin Wang, Meilin Huang, Shiang-Suo |
author_facet | Tsai, Chin-Feng Lin, Hui-Wen Liao, Jiuan-Miaw Chen, Ke-Min Tsai, Jen-Wei Chang, Chia-Sung Chou, Chia-Yu Su, Hsing-Hui Liu, Pei-Hsun Chu, Ya-Chun Wang, Yi-Hsin Wang, Meilin Huang, Shiang-Suo |
author_sort | Tsai, Chin-Feng |
collection | PubMed |
description | Myocardial ischemia/reperfusion (I/R) injury is marked by rapid increase in inflammation and not only results in myocardial apoptosis but also compromises the myocardial function. Dunaliella salina (D. salina), a halophilic unicellular microalga, has been used as a provitamin A carotenoid supplement and color additive. Several studies have reported that D. salina extract could attenuate lipopolysaccharides-induced inflammatory effects and regulate the virus-induced inflammatory response in macrophages. However, the effects of D. salina on myocardial I/R injury remain unknown. Therefore, we aimed to investigate the cardioprotection of D. salina extract in rats subjected to myocardial I/R injury that was induced by occlusion of the left anterior descending coronary artery for 1 h followed by 3 h of reperfusion. Compared with the vehicle group, the myocardial infarct size significantly decreased in rats that were pre-treated with D. salina. D. salina significantly attenuated the expressions of TLR4, COX-2 and the activity of STAT1, JAK2, IκB, NF-κB. Furthermore, D. salina significantly inhibited the activation of caspase-3 and the levels of Beclin-1, p62, LC3-I/II. This study is the first to report that the cardioprotective effects of D. salina may mediate anti-inflammatory and anti-apoptotic activities and decrease autophagy through the TLR4-mediated signaling pathway to antagonize myocardial I/R injury. |
format | Online Article Text |
id | pubmed-9963554 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99635542023-02-26 Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling Tsai, Chin-Feng Lin, Hui-Wen Liao, Jiuan-Miaw Chen, Ke-Min Tsai, Jen-Wei Chang, Chia-Sung Chou, Chia-Yu Su, Hsing-Hui Liu, Pei-Hsun Chu, Ya-Chun Wang, Yi-Hsin Wang, Meilin Huang, Shiang-Suo Int J Mol Sci Article Myocardial ischemia/reperfusion (I/R) injury is marked by rapid increase in inflammation and not only results in myocardial apoptosis but also compromises the myocardial function. Dunaliella salina (D. salina), a halophilic unicellular microalga, has been used as a provitamin A carotenoid supplement and color additive. Several studies have reported that D. salina extract could attenuate lipopolysaccharides-induced inflammatory effects and regulate the virus-induced inflammatory response in macrophages. However, the effects of D. salina on myocardial I/R injury remain unknown. Therefore, we aimed to investigate the cardioprotection of D. salina extract in rats subjected to myocardial I/R injury that was induced by occlusion of the left anterior descending coronary artery for 1 h followed by 3 h of reperfusion. Compared with the vehicle group, the myocardial infarct size significantly decreased in rats that were pre-treated with D. salina. D. salina significantly attenuated the expressions of TLR4, COX-2 and the activity of STAT1, JAK2, IκB, NF-κB. Furthermore, D. salina significantly inhibited the activation of caspase-3 and the levels of Beclin-1, p62, LC3-I/II. This study is the first to report that the cardioprotective effects of D. salina may mediate anti-inflammatory and anti-apoptotic activities and decrease autophagy through the TLR4-mediated signaling pathway to antagonize myocardial I/R injury. MDPI 2023-02-15 /pmc/articles/PMC9963554/ /pubmed/36835281 http://dx.doi.org/10.3390/ijms24043871 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Tsai, Chin-Feng Lin, Hui-Wen Liao, Jiuan-Miaw Chen, Ke-Min Tsai, Jen-Wei Chang, Chia-Sung Chou, Chia-Yu Su, Hsing-Hui Liu, Pei-Hsun Chu, Ya-Chun Wang, Yi-Hsin Wang, Meilin Huang, Shiang-Suo Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling |
title | Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling |
title_full | Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling |
title_fullStr | Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling |
title_full_unstemmed | Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling |
title_short | Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling |
title_sort | dunaliella salina alga protects against myocardial ischemia/reperfusion injury by attenuating tlr4 signaling |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9963554/ https://www.ncbi.nlm.nih.gov/pubmed/36835281 http://dx.doi.org/10.3390/ijms24043871 |
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