{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tsai CF"],"funding":["Chung Shan Medical University Hospital"],"pagination":["3871"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9963554"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(4)"],"pubmed_abstract":["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. <i>Dunaliella salina</i> (<i>D. salina</i>), a halophilic unicellular microalga, has been used as a provitamin A carotenoid supplement and color additive. Several studies have reported that <i>D. salina</i> extract could attenuate lipopolysaccharides-induced inflammatory effects and regulate the virus-induced inflammatory response in macrophages. However, the effects of <i>D. salina</i> on myocardial I/R injury remain unknown. Therefore, we aimed to investigate the cardioprotection of <i>D. salina</i> 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 <i>D. salina</i>. <i>D. salina</i> significantly attenuated the expressions of TLR4, COX-2 and the activity of STAT1, JAK2, IκB, NF-κB. Furthermore, <i>D. salina</i> 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 <i>D. salina</i> may mediate anti-inflammatory and anti-apoptotic activities and decrease autophagy through the TLR4-mediated signaling pathway to antagonize myocardial I/R injury."],"journal":["International journal of molecular sciences"],"pubmed_title":["<i>Dunaliella salina</i> Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling."],"pmcid":["PMC9963554"],"funding_grant_id":["CSH-2018-C-031","CSH-2020-C-026"],"pubmed_authors":["Chou CY","Chang CS","Huang SS","Liao JM","Tsai JW","Liu PH","Wang YH","Chen KM","Wang M","Tsai CF","Lin HW","Su HH","Chu YC"],"additional_accession":[]},"is_claimable":false,"name":"<i>Dunaliella salina</i> Alga Protects against Myocardial Ischemia/Reperfusion Injury by Attenuating TLR4 Signaling.","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. <i>Dunaliella salina</i> (<i>D. salina</i>), a halophilic unicellular microalga, has been used as a provitamin A carotenoid supplement and color additive. Several studies have reported that <i>D. salina</i> extract could attenuate lipopolysaccharides-induced inflammatory effects and regulate the virus-induced inflammatory response in macrophages. However, the effects of <i>D. salina</i> on myocardial I/R injury remain unknown. Therefore, we aimed to investigate the cardioprotection of <i>D. salina</i> 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 <i>D. salina</i>. <i>D. salina</i> significantly attenuated the expressions of TLR4, COX-2 and the activity of STAT1, JAK2, IκB, NF-κB. Furthermore, <i>D. salina</i> 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 <i>D. salina</i> may mediate anti-inflammatory and anti-apoptotic activities and decrease autophagy through the TLR4-mediated signaling pathway to antagonize myocardial I/R injury.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-04-25T22:30:27.253Z","creation":"2025-04-06T09:04:44.179Z"},"accession":"S-EPMC9963554","cross_references":{"pubmed":["36835281"],"doi":["10.3390/ijms24043871"]}}