Bioinformatics-Based Exploration of the Ability of Ginkgetin to Alleviate the Senescence of Cardiomyocytes After Myocardial Infarction and Its Cardioprotective Effects
- Han Li 1, Dongsheng Wei 2, Huimin Cao 2, Yelei Han 1, Luzhen Li 1, Yuting Liu 1, Jiajie Qi 1, Xinyue Wu 1, Zhe Zhang 2,3
- Han Li 1, Dongsheng Wei 2, Huimin Cao 2
- 1The First School of Clinical Medicine, Liaoning University of Traditional Chinese Medicine, Shenyang, 110847, People's Republic of China.
- 2Key Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang, 110847, People's Republic of China.
- 3Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, 110032, People's Republic of China.
- 0The First School of Clinical Medicine, Liaoning University of Traditional Chinese Medicine, Shenyang, 110847, People's Republic of China.
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View abstract on PubMed
Summary
This summary is machine-generated.Ginkgetin protects heart cells after myocardial infarction (MI) by reducing damage and inflammation. This study shows ginkgetin’s potential as a cardioprotective agent for treating heart attacks.
Area Of Science
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background
- Myocardial infarction (MI) is a leading cause of death globally, necessitating novel cardioprotective strategies.
- Current treatments aim to minimize cardiomyocyte damage, but more effective agents are needed.
- Ginkgo biloba extract is recognized for treating vascular and neurological conditions.
Purpose Of The Study
- To investigate the cardioprotective effects and underlying mechanisms of ginkgetin in post-myocardial infarction (MI) cardiomyocytes.
- To validate bioinformatics predictions through experimental studies.
Main Methods
- Bioinformatics analysis to predict ginkgetin's targets and pathways in MI.
- In vivo studies using a rat model of MI induced by coronary ligation.
- In vitro studies using H9c2 cardiomyocytes subjected to oxygen and glucose deprivation (OGD) to simulate ischemia.
Main Results
- Bioinformatics identified MMP2, MMP9, and VEGFA as key targets; ginkgetin may regulate immunity via the TCR signaling pathway.
- Ginkgetin ameliorated myocardial damage, cardiac dysfunction, and senescent apoptosis in vivo.
- In vitro, ginkgetin reduced OGD-induced cytotoxicity and enhanced cardiomyocyte viability.
Conclusions
- Ginkgetin demonstrates significant cardioprotective effects by inhibiting myocardial fibrosis, hypertrophy, and inflammation post-MI.
- It scavenges free radicals, suppresses inflammatory pathways, and delays cardiomyocyte senescence.
- Ginkgetin offers a promising therapeutic approach for protecting the heart after myocardial infarction.
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