Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2021, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2021/8880141
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Funding
- Chinese National Natural Science Foundation [81973435]
- Program of Collaborative Innovation Center of Chinese Medicinal Material Resources Industrialization of Jiangsu Province (2020)
- Genuine medicinal material planting and quality assurance project (2021)
- Postgraduate Research & Practice Innovation Program of Jiangsu Province [KYCX20_1496]
- Jiangsu TCM science and technology development program [YB201997]
- Blue Project Foundation of Jiangsu in 2018 for outstanding young backbone teachers
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The study demonstrated that C3G has a protective effect against myocardial ischemia-reperfusion injury by inhibiting oxidative stress and ferroptosis-related protein expression, thus highlighting its potential as a protective agent for myocardium.
This study was conducted to estimate the protective effect of Cyanidin-3-glucoside (C3G) on myocardial ischemia-reperfusion (IR) injury and to explore its mechanism. The rats were subjected to left anterior descending ligation and perfusion surgery. In vitro experiments were performed on H9c2 cells using the oxygen-glucose deprivation/reoxygenation (OGD/R) model. The results showed the administration of C3G reduced the infarction area, mitigated pathological alterations, inhibited ST segment elevation, and attenuated oxidative stress and ferroptosis-related protein expression. C3G also suppressed the expressions of USP19, Beclin1, NCOA4, and LC3II/LC3I. In addition, treatment with C3G relieved oxidative stress, downregulated LC3II/LC3I, reduced autophagosome number, downregulated TfR1 expression, and upregulated the expressions of FTH1 and GPX4 in OGD/R-induced H9c2 cells. C3G could inhibit the protein levels of USP19 and LC3II. C3G promoted K11-linked ubiquitination of Beclin1. Further evidence that C3G reduced ferroptosis and ameliorated myocardial I/R injury was demonstrated with the ferroptosis promoter RSL3. Taken together, C3G could be a potential agent to protect myocardium from myocardial I/R injury.
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