scholarly journals Protective Effects of Allicin on Acute Myocardial Infarction in Rats via Hydrogen Sulfide-mediated Regulation of Coronary Arterial Vasomotor Function and Myocardial Calcium Transport

2022 ◽  
Vol 12 ◽  
Author(s):  
Tianwei Cui ◽  
Weiyu Liu ◽  
Chenghao Yu ◽  
Jianxun Ren ◽  
Yikui Li ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Hydrogen Sulfide ◽  
Coronary Artery ◽  
Therapeutic Potential ◽  
Detection System ◽  
High Morbidity ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Vasomotor Function

Acute myocardial infarction (AMI) is a condition with high morbidity and mortality, for which effective treatments are lacking. Allicin has been reported to exert therapeutic effects on AMI, but the underlying mechanisms of its action have not been fully elucidated. To investigate this, a rat model of AMI was generated by ligating the left anterior descending branch of the coronary artery. DL-propargylglycine (PAG), a specific hydrogen sulfide (H2S) synthetase inhibitor, was used to examine the effects of allicin on H2S production. Isolated coronary arteries and cardiomyocytes were assessed for vascular reactivity and cellular Ca2+ transport using a multiwire myography system and a cell-contraction-ion detection system, respectively. Allicin administration improved cardiac function and myocardial pathology, reduced myocardial enzyme levels, and increased H2S and H2S synthetase levels. Allicin administration resulted in concentration-dependent effects on coronary artery dilation, which were mediated by receptor-dependent Ca2+ channels, ATP-sensitive K+ channels, and sarcoplasmic reticulum (SR) Ca2+ release induced by the ryanodine receptor. Allicin administration improved Ca2+ homeostasis in cardiomyocytes by increasing cardiomyocyte contraction, Ca2+ transient amplitude, myofilament sensitivity, and SR Ca2+ content. Allicin also enhanced Ca2+ uptake via SR Ca2+-ATPase and Ca2+ removal via the Na+/Ca2+ exchanger, and it reduced SR Ca2+ leakage. Notably, the protective effects of allicin were partially attenuated by blockade of H2S production with PAG. Our findings provide novel evidence that allicin-induced production of H2S mediates coronary artery dilation and regulation of Ca2+ homeostasis in AMI. Our study presents a novel mechanistic insight into the anti-AMI effects of allicin and highlights the therapeutic potential of this compound.

Upregulated miR-486 Induces Therapeutic Angiogenesis and Improves Infarction Recovery in Rat Myocardial Ischemia Model

2021 ◽  
Author(s):  
Hong-Wei Qi ◽  
Hai-Tao Zhang ◽  
Hui-Yan Sun ◽  
Lin Zhang ◽  
Yang Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Injury ◽  
Therapeutic Potential ◽  
Myocardial Infarct ◽  
Smooth Muscles ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Myocardial Repair ◽  
Acute Myocardial Infarct

Abstract BackgroundBesides hematopoietic cells, miR-486 is also enriched in cardiac, skeletal, and smooth muscles. However, its roles in regulating the function of cardiomyocytes and tissue repair in myocardial infarction have not been explored yet.MethodsWe investigated the effects of miR-486 on the survival and hypoxic response of cardiomyocytes. Also, using adenovirus-mediated overexpression, we evaluated its therapeutic effects in myocardial repair in a rat acute myocardial infarct (AMI) model.ResultsHypoxia treatment upregulated miR-486 in cardiomyocytes. Moreover, adenovirus-mediated overexpression of miR-486 reduced cell injury, increased cell viability, and decreased apoptosis in hypoxic conditions. In a rat AMI model, administration of Ad-miR-486 reduced infarct size and collagen deposition, increased vessel density, and improved cardiac function. Furthermore, in vivo data suggest that the protective effects of miR-486 in cardiomyocytes were related to its anti-apoptotic function.ConclusionmiR-486 overexpression protects myocytes from hypoxia-induced apoptosis and has therapeutic potential in myocardial infarction.

scholarly journals The Application Potential and Advance of Mesenchymal Stem Cell-Derived Exosomes in Myocardial Infarction

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Xianyun Wang ◽  
Yida Tang ◽  
Zhao Liu ◽  
Yajuan Yin ◽  
Quanhai Li ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Therapeutic Potential ◽  
Heart Function ◽  
Treatment Method ◽  
High Morbidity ◽  
Therapeutic Effects ◽  
Irreversible Loss ◽  
Free Treatment ◽  
Promising Therapeutic Approach ◽  
Application Potential

Myocardial infarction (MI) is a devastating disease with high morbidity and mortality caused by the irreversible loss of functional cardiomyocytes and heart failure (HF) due to the restricted blood supply. Mesenchymal stem cells (MSCs) have been emerging as lead candidates to treat MI and subsequent HF mainly through secreting multitudinous factors of which exosomes act as the most effective constituent to boost the repair of heart function through carrying noncoding RNAs and proteins. Given the advantages of higher stability in the circulation, lower toxicity, and controllable transplantation dosage, exosomes have been described as a wonderful and promising cell-free treatment method in cardiovascular disease. Nowadays, MSC-derived exosomes have been proposed as a promising therapeutic approach to improve cardiac function and reverse heart remodeling. However, exosomes’ lack of modification cannot result in desired therapeutic effect. Hence, optimized exosomes can be developed via various engineering methods such as pharmacological compound preconditioned MSCs, genetically modified MSCs, or miRNA-loaded exosomes and peptide tagged exosomes to improve the targeting and therapeutic effects of exosomes. The biological characteristics, therapeutic potential, and optimizing strategy of exosomes will be described in our review.

Therapeutic Potential of CXCR4/SDF-1 Axis in Acute Myocardial Infarction

2016 ◽  
Vol 1 (1) ◽  
pp. 20
Author(s):  
Shirin Hamedakbari Toosi ◽  
Javad Behravan ◽  
Asieh Heirani-Tabasi
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Therapeutic Potential

Some Problems Concerning Coronary Artery Occlusion and Acute Myocardial Infarction

Circulation ◽  
1969 ◽  
Vol 40 (5s4) ◽  
Author(s):  
DONALD B. HACKEL ◽  
E. HARVEY ESTES ◽  
ABE WALSTON ◽  
STEPHEN KOFF ◽  
EUGENE DAY
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion

scholarly journals Study of vitamin D receptor gene polymorphisms in a cohort of myocardial infarction patients with coronary artery disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Damir Raljević ◽  
Viktor Peršić ◽  
Elitza Markova-Car ◽  
Leon Cindrić ◽  
Rajko Miškulin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Vitamin D ◽  
Coronary Artery ◽  
Vitamin D Receptor ◽  
Gene Polymorphisms ◽  
Vdr Gene ◽  
Vdr Polymorphism ◽  
Vdr Gene Polymorphisms ◽  
Vdr Polymorphisms

Abstract Background Vitamin D deficiency is associated with cardiovascular diseases, including coronary artery diseases (CAD). As vitamin D manifests its biological function through its vitamin D receptor (VDR), VDR gene polymorphisms potentially affect VDR functionality and vitamin D activity. Therefore, the objective of this study was to analyze three well-studied VDR gene polymorphisms—Fok1 (rs2228570), BsmI (rs1544410) and Taq1 (rs731236)—in a cohort of CAD patients after acute myocardial infarction. Methods In the presented cross-sectional study, 155 participants with CAD after acute myocardial infarction and 104 participants in a control group without CAD were enrolled. The participants in both groups were Caucasians of European origin. The genotyping of VDR polymorphisms rs2228570, rs1544410 and rs731236 was assessed by RT-PCR. Results The results show an association between the T/T genotype of the BsmI (rs1544410) and the G/G genotype of the Taq1 (rs731236) VDR polymorphism and CAD patients after acute myocardial infarction. There was no association between the Fok1 (rs2228570) VDR polymorphism and CAD patients after acute myocardial infarction. Conclusion The presented results suggest a potential association of the BsmI (rs1544410) and Taq1 (rs731236) VDR polymorphisms with CAD patients after myocardial infarction.

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