Hydrogen gas inhalation alleviates myocardial ischemia-reperfusion injury by the inhibition of oxidative stress and NLRP3-mediated pyroptosis in rats

Nie, Chaoqun; Ding, Xue; Rong, Ao; Zheng, Min; Li, Zhenning; Pan, Shuang; Yang, Wei

doi:10.1016/j.lfs.2021.119248

Cited by 73 publications

(58 citation statements)

References 36 publications

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“…Hydrogen has been proved to possess a significant effect on the inhibition of oxidative stress, anti‐apoptosis and anti‐inflammation 10 . In the past decade, H 2 was found to exhibit treatment effects on a variety of oxidative stress and inflammation‐linked diseases, consisting of stroke, cancer, diabetes, atherosclerosis, ischaemia–reperfusion injury and neurodegenerative diseases 10‐14 . However, the effect of H 2 on long‐term cardiac remodelling and myocardial fibrosis in MI rats remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

Nie

Zou

Pan

et al. 2021

J Cellular Molecular Medi

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It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective and practical means of either prevention or treatment. Thus, novel therapeutic approaches are critical for the long‐term quality of life of individuals with myocardial ischaemia. Herein, we aimed to explore the protective effect of H2, a novel gas signal molecule with anti‐oxidative stress and anti‐inflammatory effects, on cardiac remodelling and fibrosis in MI rats, and to explore its possible mechanism. First, we successfully established MI model rats, which were then exposed to H2 inhalation with 2% concentration for 28 days (3 hours/day). The results showed that hydrogen gas can significantly improve cardiac function and reduce the area of cardiac fibrosis. In vitro experiments further proved that H2 can reduce the hypoxia‐induced damage to cardiomyocytes and alleviate angiotensin II‐induced migration and activation of cardiac fibroblasts. In conclusion, herein, we illustrated for the first time that inhalation of H2 ameliorates myocardial infarction‐induced cardiac remodelling and fibrosis in MI rats and exert its protective effect mainly through inhibiting NLRP3‐mediated pyroptosis.

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Section: Introductionmentioning

confidence: 99%

Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

Nie

Zou

Pan

et al. 2021

J Cellular Molecular Medi

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“…Recently, an increasing number of studies have demonstrated that NLRP3 inflammasome-mediated pyroptosis is emerging as a novel target to attenuate myocardial IRI (Ding et al, 2020;Nie et al, 2021). Inhibiting microRNA-29a can alleviate FIGURE 8 | Ex vivo heart perfusion combined with melatonin post-conditioning exerts a profound cardioprotective effect against myocardial IRI in the DCD heart, and this protection appears to be due to the inhibition of NLRP3 inflammasome-mediated pyroptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, an increasing number of studies have demonstrated that NLRP3 inflammasome-mediated pyroptosis is emerging as a novel target to attenuate myocardial IRI ( Ding et al, 2020 ; Nie et al, 2021 ). Inhibiting microRNA-29a can alleviate myocardial IRI in mice by targeting SIRT1 and suppressing oxidative stress and the NLRP3-mediated pyroptosis pathway ( Ding et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…Inhibiting microRNA-29a can alleviate myocardial IRI in mice by targeting SIRT1 and suppressing oxidative stress and the NLRP3-mediated pyroptosis pathway ( Ding et al, 2020 ). Furthermore, hydrogen gas inhalation can attenuate myocardial IRI in rats by the inhibition of oxidative stress and NLRP3-mediated pyroptosis ( Nie et al, 2021 ). Notably, Quader et al (2020) reported that the DCD procedure resulted in the activation of the NLRP3 inflammasome, which contributed to myocardial damage and dysfunction, while NLRP3 inflammasome inhibition ameliorated myocardial warm ischemia injury and improved DCD heart function.…”

Section: Discussionmentioning

confidence: 99%

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Normothermic ex vivo Heart Perfusion Combined With Melatonin Enhances Myocardial Protection in Rat Donation After Circulatory Death Hearts via Inhibiting NLRP3 Inflammasome-Mediated Pyroptosis

Zeng

et al. 2021

Front. Cell Dev. Biol.

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ObjectiveThe adoption of hearts from donation after circulatory death (DCD) is a promising approach for the shortage of suitable organs in heart transplantation. However, DCD hearts suffer from serious ischemia/reperfusion injury (IRI). Recent studies demonstrate that nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-mediated pyroptosis is a novel target to ameliorate myocardial IRI. Melatonin is shown to inhibit NLRP3 inflammasome-mediated pyroptosis. Therefore, this study is designed to verify the hypothesis that melatonin can protect the heart graft preserved with ex vivo heart perfusion (EVHP) against myocardial IRI via inhibiting NLRP3 inflammasome-mediated pyroptosis in a rat model of DCD.MethodsDonor-heart rats were randomly divided into three groups: (1) Control group: non-DCD hearts were harvested from heart-beating rats and immediately preserved with allogenic blood-based perfusate at constant flow for 105 min in the normothermic EVHP system; (2) DCD-vehicle group; and (3) DCD-melatonin group: rats were subjected to the DCD procedure with 25 min of warm ischemia injury and preserved by the normothermic EVHP system for 105 min. Melatonin (200 μmol/L) or vehicle was perfused in the cardioplegia and throughout the whole EVHP period. Cardiac functional assessment was performed every 30 min during EVHP. The level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis of heart grafts submitted to EVHP were evaluated.ResultsTwenty five-minute warm ischemia injury resulted in a significant decrease in the developed pressure (DP), dP/dtmax, and dP/dtmin of left ventricular of the DCD hearts, while the treatment with melatonin significantly increased the DP, dP/dtmax of the left ventricular of DCD hearts compared with DCD-vehicle group. Furthermore, warm ischemia injury led to a significant increase in the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis in the hearts preserved with EVHP. However, melatonin added in the cardioplegia and throughout the EVHP period significantly attenuated the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis compared with DCD-vehicle group.ConclusionEVHP combined with melatonin post-conditioning attenuates myocardial IRI in DCD hearts by inhibiting NLRP3 inflammasome-mediated pyroptosis, which might expand the donor pool by the adoption of transplantable DCD hearts.

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“…hypoxia/reoxygenation(HR)-induced tissue injury progress stepwise involving the ischemia and reperfusion phases. The no-re ow phenomenon seriously endangers the therapeutic effect of reperfusion therapy [2]. Therefore, it is of great importance to nd an effective and secure therapeutic solution to reduce the myocardial HR injury.…”

Section: Introductionmentioning

confidence: 99%

Mongolian Medicinal Formula Anshen-Buxin-Liuwei Pill Alleviate Cardiomyocyte Hypoxia/Reoxygenation Injury via Mitochondrion Pathway

Huang

Tong

Huang

et al. 2021

Preprint

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Anshen Buxin Liuwei pill (ABLP), a Mongolian medicinal formula, composed of the six medicinal materials of Mongolian medicine Bos taurus domesticus Gmelin, Choerospondias axillaris (Roxb. ) Burtt et Hill, Myristica fragrans Houtt., Eugenia caryophµllata Thunb., Aucklandia lappa Decne., Liqui dambar formosana Hance, is considered to have a therapeutic effect on the symptoms such as coronary heart disease, angina pectoris, arrhythmia, depression and irritability, palpitation, and shortness of breath. Therefore, the present study was employed a network pharmacology approach to identify the potentially active ingredients and to evaluate the protective effect of ABLP on hypoxia/reoxygenation (HR)-induced H9c2 cardiomyocytes, and its influence on cell viability, apoptosis, oxidative stress. H9c2 cardiomyocytes were used to construct a HR injury model. CCK-8 assay and AnnexinV-FITC cell apoptosis assays were used for cell viability and cell apoptosis determination. The levels of LDH, SOD, MDA, CAT, CK, GSH-Px, Na+-K+-ATPase, and Ca2+-ATPase in the cells were determined to assess the effect of ABLP. the mRNA levels of Sirtuin3 (Sirt3) and Cytochrome C (Cytc) in H9c2 cells were determined by quantitative real-time PCR. The finding of this study indicates that HR treatment cells began to shrink from the spindle in an irregular shape with some floated in the medium, well by increasing the therapeutic dose of ABLP (5 µg/mL, 25 µg/mL, and 50 µg/mL), the cells gradually reconverted in a concentration-dependent manner. The release of CK in HR-treated cells was significantly increased, indicating that ABLP exerts a protective effect in H9c2 cells against HR injury and can improve the mitochondrial energy metabolism and mitochondrial function integrity. The present study scrutinized the cardio-protective effect of ABLP against the HR-induced H9c2 cells injury through antioxidant and mitochondrion pathways. ABLP could be a promising therapeutic drug for the treatment of myocardial ischemic cardiovascular disease. The results will provide reasonable information for clinical use of the ABLP.

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Hydrogen gas inhalation alleviates myocardial ischemia-reperfusion injury by the inhibition of oxidative stress and NLRP3-mediated pyroptosis in rats

Cited by 73 publications

References 36 publications

Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

Normothermic ex vivo Heart Perfusion Combined With Melatonin Enhances Myocardial Protection in Rat Donation After Circulatory Death Hearts via Inhibiting NLRP3 Inflammasome-Mediated Pyroptosis

Mongolian Medicinal Formula Anshen-Buxin-Liuwei Pill Alleviate Cardiomyocyte Hypoxia/Reoxygenation Injury via Mitochondrion Pathway

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