Effect of hydrogen-rich water on the Nrf2/ARE signaling pathway in rats with myocardial ischemia-reperfusion injury

Li, Liangtong; Liu, Tongtong; Liu, Li; Li, Shaochun; Zhang, Zhe; Zhang, Ruisha; Zhou, Yujuan; Liu, Fulin

doi:10.1007/s10863-019-09814-7

Cited by 35 publications

(21 citation statements)

References 38 publications

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“…Coronary heart disease is one of the leading causes of death and disability worldwide [ 13 ]. The main treatment methods are drugs, percutaneous coronary intervention, and coronary artery bypass grafting.…”

Section: Discussionmentioning

confidence: 99%

[Retracted] CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia‐Reperfusion Injury via Inhibiting miRNA‐133 Expression

Zong

Wang

2020

BioMed Research International

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Objective. This project is aimed at investigating whether CircANXA2 can promote the apoptosis of myocardial cells by inhibiting miR-133 expression and thereby participate in the development of myocardial ischemia-reperfusion injury. Materials and Method. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of CircANXA2 in H9c2 cells after hypoxia/reoxygenation (H/R) treatment. Evaluation of myocardial injury markers in H9c2 cells was performed using commercial kits, including lactate dehydrogenase (LDH), malonaldehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidation (GSH-PX). MTT analysis and flow cytometry were used to detect myocardial cell proliferation and apoptosis, respectively. Western blot was used to detect the protein expression of apoptosis-related genes. Result. qRT-PCR results showed that compared with the control, the expression of CircANXA2 was upregulated and the expression level of miR-133 was significantly decreased in H/R-treated H9c2 cells. CircANXA2 overexpression increased LDH, MDA, SOD, and GSH-PX activity in H/R-treated H9c2 cells. At the same time, CircANXA2 overexpression inhibited the proliferation of H/R-treated cells, and CircANXA2 was able to induce cardiomyocyte apoptosis. Western blot results showed that after overexpression of CircANXA2, the proapoptotic genes Bax and cytochrome C was upregulated, while the antiapoptotic gene Bcl-2 was downregulated. In H9c2 cells, upregulating miR-133 can reverse the inhibition of proliferation induced by CircANXA2 overexpression and increase apoptosis. Conclusions. CircANXA2 promotes cardiomyocyte apoptosis in myocardial ischemia-reperfusion injury by inhibiting the expression of miR-133. CircANXA2 may be a potential target for myocardial ischemia-reperfusion injury.

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Section: Discussionmentioning

confidence: 99%

[Retracted] CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia‐Reperfusion Injury via Inhibiting miRNA‐133 Expression

Zong

Wang

2020

BioMed Research International

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“…Other studies demonstrated that intraperitoneal injection of HW before reperfusion significantly decreased the concentration of malondialdehyde (MDA) and infarct size, as well as reducing myocardial 8-OHdG and the levels of TNF- α and IL-1 β in an area at risk zones [ 92 , 93 ]. Moreover, Qian et al described the hydrogen-mediated protection of myocardium degeneration due to radiation-induced injury in rats [ 94 ]. Treatment with HRS was shown to ameliorate vascular dysfunction, including aortic hypertrophy and endothelial function, in spontaneously hypertensive rats by abating oxidative stress, restoring baroreflex function, preserving mitochondrial function, and enhancing nitric oxide bioavailability [ 95 ].…”

Section: Preventive and Therapeutic Applications Of H 2 mentioning

confidence: 99%

Hydrogen: A Novel Option in Human Disease Treatment

Yang

Dong

et al. 2020

Oxidative Medicine and Cellular Longevity

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H2 has shown anti-inflammatory and antioxidant ability in many clinical trials, and its application is recommended in the latest Chinese novel coronavirus pneumonia (NCP) treatment guidelines. Clinical experiments have revealed the surprising finding that H2 gas may protect the lungs and extrapulmonary organs from pathological stimuli in NCP patients. The potential mechanisms underlying the action of H2 gas are not clear. H2 gas may regulate the anti-inflammatory and antioxidant activity, mitochondrial energy metabolism, endoplasmic reticulum stress, the immune system, and cell death (apoptosis, autophagy, pyroptosis, ferroptosis, and circadian clock, among others) and has therapeutic potential for many systemic diseases. This paper reviews the basic research and the latest clinical applications of H2 gas in multiorgan system diseases to establish strategies for the clinical treatment for various diseases.

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“…Chu 33 et al Ginsenoside Rg1 plays a protective role in I/R injury and alleviates neuron injury by regulating miR-144/Nrf2/are pathway. Li 34 et al Hydrogen rich water can alleviate I/R-induced cardiac injury and effectively reduce the occurrence of oxidative stress by regulating Nrf2/ARE signaling pathway. In this study, we speculated that pravastatin may alleviate I/R injury by regulating Nrf2/ARE signaling pathway.…”

Section: Dovepressmentioning

confidence: 99%

<p>Protective Effect of Pravastatin on Myocardial Ischemia Reperfusion Injury by Regulation of the miR-93/Nrf2/ARE Signal Pathway</p>

Liu¹,

Zhang²,

Zhao³

et al. 2020

DDDT

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Purpose: This research intended to study the mechanism of pravastatin in myocardial ischemia reperfusion (I/R) injury. Patients and Methods: Altogether 70 male rats were selected and grouped into Sham operation group (Sham group), ischemia reperfusion group (I/R group), pravastatin pretreatment group (I/R+P group), I/R+miR-93-mimics, I/R+P+miR-93-mimics, I/R+Nrf2 siRNA, and I/R+P+Nrf2 siRNA group. The myocardial function of each group was detected. Results: Myocardial I/R injury could lead to abnormal myocardial enzyme activity, inflammatory reaction and oxidative stress. However, pravastatin could significantly inhibit the activity of myocardial enzymes, alleviate inflammatory reaction and inhibit oxidative stress reaction, thus playing a protective role. Furthermore, cell experiments showed that pravastatin can alleviate the injury of H9C2 myocardial cells caused by I/R, inhibit the apoptosis of myocardial cells, and lead to a significant reduction in pro-apoptotic genes Bax, caspase-3 and caspase-9 transcription levels, an obvious increase in anti-apoptotic gene Bcl-2, and an increase in cell activity. After I/R induced injury, miR-93 level was significantly up-regulated and Nrf2 level was down-regulated. Over-expression of miR-93 or inhibition of Nrf2 expression would lead to further aggravation of I/R myocardial injury, increase the apoptosis rate of cells and decrease the activity of myocardial cells. Pravastatin administration could inhibit miR-93, activate and promote Nrf2 in myocardial tissue, and promote protein expression of downstream regulatory genes HO-1 and NQO1. In the I/R model, pravastatin was given. Over-expression of miR-93 or silencing Nrf2 could reverse the therapeutic effect of pravastatin on I/R. Conclusion: Pravastatin acts as a protector on myocardial ischemia reperfusion injury by regulating miR-93/Nrf2/ARE signaling pathway.

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Effect of hydrogen-rich water on the Nrf2/ARE signaling pathway in rats with myocardial ischemia-reperfusion injury

Cited by 35 publications

References 38 publications

[Retracted] CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia‐Reperfusion Injury via Inhibiting miRNA‐133 Expression

[Retracted] CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia‐Reperfusion Injury via Inhibiting miRNA‐133 Expression

Hydrogen: A Novel Option in Human Disease Treatment

<p>Protective Effect of Pravastatin on Myocardial Ischemia Reperfusion Injury by Regulation of the miR-93/Nrf2/ARE Signal Pathway</p>

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