THE STABLE HYDROGEN SULFIDE DONOR, DIALLYL TRISULFIDE, PROTECTS AGAINST ACUTE MYOCARDIAL INFARCTION IN MICE

It has now become universally accepted that hydrogen sulfide (H2S), previously considered only as a lethal toxin, has robust cytoprotective actions in multiple organ systems. The diverse signaling profile of H2S impacts multiple pathways to exert cytoprotective actions in a number of pathological states. This paper will review the recently described cardioprotective actions of hydrogen sulfide in both myocardial ischemia/reperfusion injury and congestive heart failure.

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Cardioprotective effects and pharmacokinetic properties of a controlled release formulation of a novel hydrogen sulfide donor in rats with acute myocardial infarction

Bioscience Reports ◽

10.1042/bsr20140185 ◽

2015 ◽

Vol 35 (3) ◽

Cited By ~ 7

Author(s):

Ba Hieu Tran ◽

Chengrong Huang ◽

Qiuyan Zhang ◽

Xu Liu ◽

Shizhou Lin ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Hydrogen Sulfide ◽

Controlled Release ◽

Cardiovascular Diseases ◽

Release Formulation ◽

Controlled Release Formulation ◽

Pharmacokinetic Properties ◽

Cardioprotective Effects

The present study confirms that CR-SPRC is stable, effective and is thus an alternative candidate for hydrogen sulfide-mediated long-term prevention of cardiovascular diseases.

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S-allylcysteine mediates cardioprotection in an acute myocardial infarction rat model via a hydrogen sulfide-mediated pathway

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00853.2007 ◽

2007 ◽

Vol 293 (5) ◽

pp. H2693-H2701 ◽

Cited By ~ 92

Author(s):

Shin Chet Chuah ◽

Philip K. Moore ◽

Yi Zhun Zhu

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Hydrogen Sulfide ◽

Cardiovascular Diseases ◽

Treated Group ◽

Left Ventricular ◽

Rat Models ◽

Expression Studies ◽

Group Protein ◽

Related Pathway

S-allylcysteine (SAC) is an organosulfur-containing compound derived from garlic. Studies have shown that garlic is beneficial in the treatment of cardiovascular diseases. This study aims to elucidate if SAC is responsible for this cardioprotection using acute myocardial infarction (AMI) rat models. In addition, we hypothesized that SAC may mediate cardioprotection via a hydrogen sulfide (H2S)-related pathway. Rats were pretreated with saline, SAC (50 mg·kg−1·day−1), SAC + propagylglycine (PAG; 50 mg + 10 mg·kg−1·day−1) or PAG (10 mg·kg−1·day−1) for 7 days before AMI induction and killed 48 h after. Our results showed that SAC significantly lowered mortality (12.5% vs. 33.3%, P < 0.05) and reduced infarct size. SAC + PAG- and PAG-treated rats had larger infarct sizes than controls (60.9 ± 0.01 and 62.0 ± 0.03%, respectively, vs. 50.0 ± 0.03%; P < 0.05). Pretreatment with SAC did not affect BP, but BP was significantly elevated in SAC + PAG and PAG-treated groups ( P < 0.05). In addition, plasma H2S levels and left ventricular cystathionine-γ-lyase (CSE) activities were analyzed to investigate the involvement of H2S. CSE is the enzyme responsible for H2S production in the heart. SAC increased left ventricular CSE activity in AMI rats (2.75 ± 0.34 vs. 1.23 ± 0.16 μmol·g protein−1·h−1; P < 0.01). SAC + PAG-treated rats had significantly lower CSE activity compared with the SAC-treated group (1.22 ± 0.27 vs. 2.75 ± 0.34 μmol·g protein−1·h−1; P < 0.05). Similarly, SAC-treated rats had higher plasma H2S concentration compared with controls and the SAC + PAG-treated group. Protein expression studies revealed that SAC upregulated CSE expression (1.1-fold of control; P < 0.05), whereas SAC + PAG and PAG downregulated its expression (0.88-fold of control in both groups; P < 0.005). In conclusion, our study provides novel evidence that SAC is protective in myocardial infarction via an H2S-related pathway.

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Exogenous hydrogen sulfide inhibits apoptosis by regulating endoplasmic reticulum stress–autophagy axis and improves myocardial reconstruction after acute myocardial infarction

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmaa133 ◽

2020 ◽

Vol 52 (12) ◽

pp. 1325-1336

Author(s):

Yaling Li ◽

Maojun Liu ◽

Jiali Yi ◽

Xiong Song ◽

Xia Zheng ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Endoplasmic Reticulum ◽

Hydrogen Sulfide ◽

Er Stress ◽

Inhibitory Effect ◽

Myocardial Apoptosis ◽

Apoptosis Protein ◽

Related Proteins

Abstract During acute myocardial infarction, endoplasmic reticulum (ER) stress-induced autophagy and apoptosis have been shown as important pathogeneses of myocardial reconstruction. Importantly, hydrogen sulfide (H2S), as a third endogenous gas signaling molecule, exerts strong cytoprotective effect on anti-ER stress, autophagy regulation and antiapoptosis. Here, we showed that H2S treatment inhibits apoptosis by regulating ER stress–autophagy axis and improves myocardial reconstruction after acute myocardial infarction. We found that H2S intervention improved left ventricle function, reduced glycogen deposition in myocardial tissue mesenchyme, and inhibited apoptosis. Moreover, the expressions of fibrosis indicators (Col3a1 and Col1a2), ER stress-related proteins (CHOP and BIP/ERP78), autophagy-related proteins (Beclin and ATG5), apoptosis protein (Bax), as well as fibrosis protein Col4a3bp were all decreased after treatment with H2S. H2S administration also maintained MMP/TIMP balance. Mechanistically, H2S activated the PI3K/AKT signaling pathway. In addition, H2S treatment also reduced the expressions of ER stress–related proteins, autophagy-related proteins, and apoptins in in vitro experiments. Interestingly, activation of ER stress–autophagy axis could reverse the inhibitory effect of H2S on myocardial apoptosis. Altogether, these results suggested that exogenous H2S suppresses myocardial apoptosis by blocking ER stress–autophagy axis, which in turn reverses cardiac remodeling after myocardial infarction.

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

Frontiers in Pharmacology ◽

10.3389/fphar.2021.752244 ◽

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.

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P11 Determination pharmacokinetic properties and cardioprotective effects of a novel hydrogen sulfide agent – Controlled release formulation of S-propargyl-cysteine on acute myocardial infarction rats

Nitric Oxide ◽

10.1016/j.niox.2014.03.061 ◽

2014 ◽

Vol 39 ◽

pp. S19

Author(s):

BaHieu Tran ◽

Shujun Wang ◽

Yi-Zhun Zhu

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Hydrogen Sulfide ◽

Controlled Release ◽

Release Formulation ◽

Controlled Release Formulation ◽

Pharmacokinetic Properties ◽

Cardioprotective Effects

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An electron microscopic study of the intra-myocardial lesions in cases of acute myocardial infarction

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010008328x ◽

1978 ◽

Vol 36 (2) ◽

pp. 484-485

Author(s):

Masahiro Ono ◽

Kaoru Aihara ◽

Gompachi Yajima

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Coronary Vessels ◽

Vascular Wall ◽

Vascular Changes ◽

Electron Microscopic ◽

Main Trunk ◽

Mechanical Destruction ◽

Transmission Electron ◽

Myocardial Lesions

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.

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