2021
DOI: 10.1016/j.biopha.2020.110970
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Effects of ω-3 PUFA and ascorbic acid combination on post-resuscitation myocardial function

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Cited by 14 publications
(11 citation statements)
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“…Since previous research suggested that ω-3 PUFA has some protective effects related to cardiac arrest, we were excited about this realization. In our next step (Cheng et al, 2020), we verified in vivo that ω-3 statistically significantly improved postresuscitation myocardial dysfunction, which corresponds specifically to our collected data. We showed that the FIGURE 1 | UPLC-HRMS/MS measures metabolite levels in plasma samples.…”
Section: Introductionsupporting
confidence: 81%
“…Since previous research suggested that ω-3 PUFA has some protective effects related to cardiac arrest, we were excited about this realization. In our next step (Cheng et al, 2020), we verified in vivo that ω-3 statistically significantly improved postresuscitation myocardial dysfunction, which corresponds specifically to our collected data. We showed that the FIGURE 1 | UPLC-HRMS/MS measures metabolite levels in plasma samples.…”
Section: Introductionsupporting
confidence: 81%
“…The three routes of administration produced similar cardioprotective effects against oxidative stress induced by IRI [ 124 ]. In addition, Cheng et al showed that it helps to reduce the inflammatory response in addition to reducing oxidative stress and heart IRI [ 125 ].…”
Section: Therapies For Myocardial Reperfusion Injurymentioning
confidence: 99%
“…Furthermore, other studies demonstrated that n-3 PUFA treatment significantly reduced lipid peroxidation by measuring MDA levels and increased the activity of antioxidant enzymes such as SOD in the myocardium. These facts suggest that n-3 PUFA may improve cardioprotection and prevent IRI due to the attenuation of oxidative damage and its anti-inflammatory activity [ 125 ].…”
Section: Therapies For Myocardial Reperfusion Injurymentioning
confidence: 99%
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“…General application of antioxidant therapies, such as vitamin C, α-tocopherol, and edaravone, have shown attenuation of ROS in preclinical and some clinical settings ( 43 45 ). Although there are multiple ongoing clinical trials evaluating the beneficial effects of antioxidant therapies in human CA patients, the mixed beneficial evidence from the preclinical setting does not support the translation of these singular antioxidant therapies ( 46 48 ). Site-specific inhibitors of ROS are more promising candidates because (1) they directly control the release of ROS at the source and (2) ROS generation at different sites can play either a beneficial, or a detrimental role ( 49 ).…”
Section: Overview Of the Various Cardiac Arrest-mediated Pathway Alterationsmentioning
confidence: 99%