Ozone protects cardiomyocytes against ischemia/reperfusion injury: Regulating the heat shock protein 70 (HSP70) expression through activating the JAK2/STAT3 Pathway

Yu, Shenglong; Guo, Huizhuang; Luo, Yi; Chen, Hanwei

doi:10.1080/21655979.2021.1974760

Cited by 10 publications

(8 citation statements)

References 48 publications

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“…The JAK–STATs signaling pathway has been shown to play a role in a variety of biological processes, including cell activation, proliferation, differentiation, autophagy, and apoptosis [ 27 ], and the activation of JAK2–STAT3 is involved in the protection of myocardial tissue [ 28 ]. However, whether the protective effect of JAK2–STAT3 is associated with amelioration of oxidative stress and the relationship of OMT with JAK2–STAT3 signaling are unclear.…”

Section: Resultsmentioning

confidence: 99%

Oxymatrine ameliorates myocardial injury by inhibiting oxidative stress and apoptosis via the Nrf2/HO-1 and JAK/STAT pathways in type 2 diabetic rats

Huang

Long

et al. 2023

BMC Complement Med Ther

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The necessity of increasing the efficiency of organ preservation has encouraged researchers to explore the mechanisms underlying diabetes-related myocardial injuries. This study intended to evaluate the protective effects of oxymatrine (OMT) in myocardial injury caused by type 2 diabetes mellitus. A model of diabetic rats was established to simulate type 2 diabetes mellitus using an intraperitoneal injection of a single dose of 65 mg/kg streptozotocin with a high-fat and high-cholesterol diet, and diabetic rats were subsequently treated with OMT (60, 120 mg/kg) by gavage for 8 weeks. Thereafter, diabetic rats demonstrated notable decreases in left ventricular systolic pressure (LVSP), ±dp/dtmax, and in the activities of glutathione peroxidase, superoxide dismutase, and catalase. Moreover, we found notable increases in left ventricular end-diastolic pressure, fasting blood glucose, and malondialdehyde, as well as changes in cell apoptosis and decreased expression levels of Nrf2, HO-1, tyrosine protein kinase JAK (JAK), and signal transducer and transcription activator (STAT). Treatment with OMT alleviated all of the measured parameters. Collectively, these findings suggest that activation of the Nrf2/HO-1 and inhibition of the JAK/STAT signaling are involved in mediating the cardioprotective effects of OMT and also highlight the benefits of OMT in ameliorating myocardial injury in diabetic rats.

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Section: Resultsmentioning

confidence: 99%

Oxymatrine ameliorates myocardial injury by inhibiting oxidative stress and apoptosis via the Nrf2/HO-1 and JAK/STAT pathways in type 2 diabetic rats

Huang

Long

et al. 2023

BMC Complement Med Ther

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“…123 Ozone uses the same mechanism of the JAK/STAT3 pathway to prevent ischemia/reperfusion injury, by regulating the production of the heat shock protein hsp70, thus assuming even a cardioprotective role. 124 Finally, some evidence reported that ozone can modify, by oxidation, the biochemistry of fibrinogen, so impairing its function. 125 According to the existing literature and our calculations, this occurs with ozone doses sensitively higher than the ones used in the ozone therapy protocols.…”

Section: Effect Of Ozone Therapy On Coagulation and Fibrinolysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ozone in the adjunct medical treatment. The round personality of a molecule with hormetic properties

Chirumbolo,

Tirelli,

Franzini

et al. 2023

Hum Exp Toxicol

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Ozone, an allotrope of oxygen, is enjoying an increasing interest in the setting and management of the medical adjunct treatment, which is called, maybe too simplistically, “ozone therapy”. Ozone is not a medicine, so the word therapy does not properly fit this gaseous molecule. Like many natural compounds, for example plant flavonoids, even ozone interacts with aryl hydrocarbon receptors (AhRs) and, at low doses, it works according to the paradoxical mechanism of hormesis, involving mitochondria (mitohormesis). Ozone, in the hormetic range, exerts cell protective functions via the Nrf2-mediated activation of the anti-oxidant system, then leading to anti-inflammatory effects, also via the triggering of low doses of 4-HNE. Moreover, its interaction with plasma and lipids forms reactive oxygen species (ROS) and lipoperoxides (LPOs), generally called ozonides, which are enabled to rule the major molecular actions of ozone in the cell. Ozone behaves as a bioregulator, by activating a wide population of reactive intermediates, which usually target mitochondria and their turnover/biogenesis, often leading to a pleiotropic spectrum of actions and behaving as a tuner of the fundamental mechanisms of survival in the cell. In this sense, ozone can be considered a novelty in the medical sciences and in the clinical approach to pharmacology and medical therapy, due to its ability to target complex regulatory systems and not simple receptors.

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“…It is considered a cardioprotective factor owing to its activation of antioxidant enzymes and induction of anti-apoptotic proteins [ 16 ]. STAT3 activation protects cardiomyocytes from ischemia-reperfusion injury [ 17 ]. High expression of STAT3 helps cardiomyocytes in tolerating H 2 O 2 stimulation, and hence, decreases apoptosis [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Bone morphogenetic protein 10 alleviates doxorubicin-induced cardiac injury via signal transducer and activator of transcription 3 signaling pathway

Fan

Guo

et al. 2022

Bioengineered

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Doxorubicin (DOX) has limited antitumor applications owing to its association with life-threatening cardiac injury. Oxidative damage and cardiac apoptosis are crucial in DOX-induced cardiac injury. Bone morphogenetic protein 10 (BMP10) is predominantly distributed in the heart and acts as a cardioprotective factor that preserves cardiac function. However, the role of BMP10 in DOX-induced cardiac injury has not yet been explored. The current study aimed to examine the function and mechanism of action of BMP10 in DOX-induced cardiac injury. An adeno-associated viral system was used for the overexpression or silencing of cardiac-specific BMP10, and subsequently, a single dose of DOX was intraperitoneally injected to induce cardiac injury. Results showed that DOX exposure decreased BMP10 expression in the heart. Cardiac-specific overexpression of BMP10 alleviated the oxidative stress and apoptosis and improved cardiac function. Conversely, cardiac-specific silencing of BMP10 aggravated the redox disorder and apoptosis and worsened the cardiac dysfunction caused by DOX. Exogenous BMP10 supplementation amelioratesd the DOX-induced cardiac contractile dysfunction. Mechanistically, we found that phosphorylation of signal transducer and activator of transcription 3 (STAT3) is reduced in DOX-induced cardiotoxicity, and, BMP10 activated impaired STAT3 via a non-canonical pathway. BMP10 lost its cardioprotective function in cardiomyocyte-specific STAT3 knockout (STAT3-cKO) mice. Based on our findings, we suggested that BMP10 is a potential therapeutic agent against DOX-induced cardiac injury and that the cardioprotective effects of BMP10 are dependent on the activation of STAT3.

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Ozone protects cardiomyocytes against ischemia/reperfusion injury: Regulating the heat shock protein 70 (HSP70) expression through activating the JAK2/STAT3 Pathway

Cited by 10 publications

References 48 publications

Oxymatrine ameliorates myocardial injury by inhibiting oxidative stress and apoptosis via the Nrf2/HO-1 and JAK/STAT pathways in type 2 diabetic rats

Oxymatrine ameliorates myocardial injury by inhibiting oxidative stress and apoptosis via the Nrf2/HO-1 and JAK/STAT pathways in type 2 diabetic rats

Ozone in the adjunct medical treatment. The round personality of a molecule with hormetic properties

Bone morphogenetic protein 10 alleviates doxorubicin-induced cardiac injury via signal transducer and activator of transcription 3 signaling pathway

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