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  2. College of Medicine /醫學院
  3. School of Medicine /醫學系
  4. Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling
 
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Dunaliella salina Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling

Journal
International Journal of Molecular Sciences
Journal Volume
24
Journal Issue
4
Start Page
3871
ISSN
1422-0067
Date Issued
2023-02-15
Author(s)
Chin-Feng Tsai  
Hui-Wen Lin  
Jiuan-Miaw Liao
Ke-Min Chen  
Jen-Wei Tsai
Chia-Sung Chang
Chia-Yu Chou
Hsing-Hui Su  
Pei-Hsun Liu
Ya-Chun Chu
Yi-Hsin Wang  
Meilin Wang
Shiang-Suo Huang  
DOI
10.3390/ijms24043871
URI
https://scholars.csmu.edu.tw/handle/123456789/4696
Abstract
<jats:p>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.</jats:p>
Publisher
MDPI AG
Type
journal-article
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