Hydrogen-Rich Saline Attenuates Lipopolysaccharide-Induced Heart Dysfunction by Restoring Fatty Acid Oxidation in Rats by Mitigating c-Jun n-Terminal Kinase Activation

Tao, Bingdong; Liu, Lidan; Wang, Ni; Tong, Dongyi; Wang, Wei; Zhang, Jin

doi:10.1097/shk.0000000000000467

Cited by 15 publications

(20 citation statements)

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“…Moreover, our findings also confirmed that inhalation of H 2 was able to improve cardiac function which was also verified by hemodynamic measurement. Furthermore, the safety of molecular hydrogen to cardiomyocytes has been confirmed as reported before ( Tao et al, 2015 ). However, in our previous study, LVEDD in saline, doxorubicin and doxorubicin+hydrogen-rich saline groups was not found differences ( Gao et al, 2017 ).…”

Section: Discussionsupporting

confidence: 82%

Inhalation of Hydrogen Attenuates Progression of Chronic Heart Failure via Suppression of Oxidative Stress and P53 Related to Apoptosis Pathway in Rats

Chi

Hong

et al. 2018

Front. Physiol.

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Background: Continuous damage from oxidative stress and apoptosis are the important mechanisms that facilitate chronic heart failure (CHF). Molecular hydrogen (H2) has potentiality in the aspects of anti-oxidation. The objectives of this study were to investigate the possible mechanism of H2 inhalation in delaying the progress of CHF.Methods and Results: A total of 60 Sprague-Dawley (SD) rats were randomly divided into four groups: Sham, Sham treated with H2, CHF and CHF treated with H2. Rats from CHF and CHF treated with H2 groups were injected isoprenaline subcutaneously to establish the rat CHF model. One month later, the rat with CHF was identified by the echocardiography. After inhalation of H2, cardiac function was improved vs. CHF (p < 0.05), whereas oxidative stress damage and apoptosis were significantly attenuated (p < 0.05). In this study, the mild oxidative stress was induced in primary cardiomyocytes of rats, and H2 treatments significantly reduced oxidative stress damage and apoptosis in cardiomyocytes (p < 0.05 or p < 0.01). Finally, as a pivotal transcription factor in reactive oxygen species (ROS)-apoptosis signaling pathway, the expression and phosphorylation of p53 were significantly reduced by H2 treatment in this rat model and H9c2 cells (p < 0.05 or p < 0.01).Conclusion: As a safe antioxidant, molecular hydrogen mitigates the progression of CHF via inhibiting apoptosis modulated by p53. Therefore, from the translational point of view and speculation, H2 is equipped with potential therapeutic application as a novel antioxidant in protecting CHF in the future.

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Section: Discussionsupporting

confidence: 82%

Inhalation of Hydrogen Attenuates Progression of Chronic Heart Failure via Suppression of Oxidative Stress and P53 Related to Apoptosis Pathway in Rats

Chi

Hong

et al. 2018

Front. Physiol.

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“…Since the first report in 2007, (5) accumulating evidence has demonstrated its therapeutic potential against IRI and the underlying mechanisms therein. Currently, H 2 i s known to have 3 definitive effects: antioxidant, (5)(6)(7)(8)(9)(10)(11)(12)(13) anti-inflammatory, (10,(14)(15)(16) and antiapoptosis. (8,17) Though some experimental animal studies have shown its therapeutic potential in organ preservation, eg, lung, (11) heart, (18) kidney, (6) intestine, (7) and liver, (19,20) its clinical use is yet to be applied because of its unfavorable features.…”

mentioning

confidence: 99%

Hydrogen Flush After Cold Storage as a New End‐Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury

Tamaki¹,

Hata²,

Okamura³

et al. 2018

Liver Transpl

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Cold storage (CS) remains the gold standard for organ preservation worldwide, although it is inevitably associated with ischemia/reperfusion injury (IRI). Molecular hydrogen (H ) is well known to have antioxidative properties. However, its unfavorable features, ie, inflammability, low solubility, and high tissue/substance permeability, have hampered its clinical application. To overcome such obstacles, we developed a novel reconditioning method for donor organs named hydrogen flush after cold storage (HyFACS), which is just an end-ischemic H flush directly to donor organs ex vivo, and, herein, we report its therapeutic impact against hepatic IRI. Whole liver grafts were retrieved from Wistar rats. After 24-hour CS in UW solution, livers were cold-flushed with H solution (1.0 ppm) via the portal vein (PV), the hepatic artery (HA), or both (PV + HA). Functional integrity and morphological damages were then evaluated by 2-hour oxygenated reperfusion at 37°C. HyFACS significantly lowered portal venous pressure, transaminase, and high mobility group box protein 1 release compared with vehicle-treated controls (P < 0.01). Hyaluronic acid clearance was significantly higher in the HyFACS-PV and -PV + HA groups when compared with the others (P < 0.01), demonstrating the efficacy of the PV route to maintain the sinusoidal endothelia. In contrast, bile production and lactate dehydrogenase leakage therein were both significantly improved in HyFACS-HA and -PV + HA (P < 0.01), representing the superiority of the arterial route to attenuate biliary damage. Electron microscopy consistently revealed that sinusoidal ultrastructures were well maintained by portal HyFACS, while microvilli in bile canaliculi were well preserved by arterial flush. As an underlying mechanism, HyFACS significantly lowered oxidative damages, thus improving the glutathione/glutathione disulfide ratio in liver tissue. In conclusion, HyFACS significantly protected liver grafts from IRI by ameliorating oxidative damage upon reperfusion in the characteristic manner with its route of administration. Given its safety, simplicity, and cost-effectiveness, end-ischemic HyFACS may be a novel pretransplant conditioning for cold-stored donor organs.

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“…By contrast, the anti-apoptotic effects of STAT3 in tumor cells may contribute to tumor growth ( 54 , 55 ). Tao et al ( 56 ) measured cardiac function in rats by echocardiography 8 h after injections of LPS and/or HRS, and observed that the addition of HRS increased fractional shortening and the ratio of phosphocreatinine to ATP. Furthermore, the potential inhibition of JNK by HRS had beneficial effects in the LPS-challenged rats, by restoring cardiac fatty acid oxidation ( 56 ).…”

Section: Discussionmentioning

confidence: 99%

“…Tao et al ( 56 ) measured cardiac function in rats by echocardiography 8 h after injections of LPS and/or HRS, and observed that the addition of HRS increased fractional shortening and the ratio of phosphocreatinine to ATP. Furthermore, the potential inhibition of JNK by HRS had beneficial effects in the LPS-challenged rats, by restoring cardiac fatty acid oxidation ( 56 ). To further investigate the underlying mechanism of the JAK2/STAT3 pathway regarding myocardial IRI, cultured myocardial cells were subjected to hypoxia and reoxygenation and JAK2 siRNA was used to specifically block the JAK2/STAT3 pathway.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen‑rich solution attenuates myocardial injury caused by cardiopulmonary bypass in rats via the Janus‑activated kinase 2/signal transducer and activator of transcription 3 signaling pathway

et al. 2018

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The incidence of complications and mortality following open-heart surgery with cardiopulmonary bypass (CPB) is associated with the severity of the myocardial injury that occurs during surgery. Hydrogen-rich solution (HRS) may prevent antioxidant stress and inhibit apoptosis and inflammation. The present study was designed to investigate the effects of HRS on CPB-induced myocardial injury, and to investigate its potential regulation of the Janus-activated kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway. The HRS treatment resulted in the significant upregulation of malonyl dialdehyde (MDA) and myeloperoxidase (MPO), whilesuperoxide dismutase (SOD) levels were significantly downregulated, compared with the Sham group (P<0.05). Additionally, HRS treatment improved myocardial injury, and decreased the expression levels of cardiac troponins, heart-type fatty acid binding protein, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, MDA and MPO, and increased SOD release in CPB rats (P<0.05). Additionally, in the CPB group without the HRS treatment, the expression levels of B-cell lymphoma (Bcl)-2, JAK2, phospho-JAK2 (p-JAK2), STAT3 and phospho-STAT3 (p-STAT3) were significantly decreased, and Bax was significantly increased, compared with the Sham group (P<0.05). By contrast, compared with the CPB group, the expression levels of B-cell lymphoma 2 (Bcl-2), JAK2, phosphorylated (p)-JAK2, STAT3 and p-STAT3 in the HRS group were significantly increased, and Bcl-2-associated X protein expression was significantly decreased (P<0.05). In JAK2 knockdown experiments using siRNA, HRS treatment following hypoxia/reoxygenation also significantly increased the viability of myocardial cells, decreased the rate of myocardial cell apoptosis, elevated the levels of SOD and suppressed the release of MDA and lactate dehydrogenase in the control siRNA and CPB groups (P<0.05). Furthermore, JAK2 siRNA attenuated these protective effects of HRS (P<0.05 vs. control siRNA, HRS and CPB groups). Additionally, the results demonstrated that the HRS treatment significantly increased the expression levels of p-JAK2, p-STAT3 and Bcl-2 in myocardial cells following hypoxia and decreased Bax expression in the control siRNA and CPB groups (P<0.05). In addition, JAK2 siRNA was determined to attenuate these effects of HRS (P<0.05 vs. control siRNA, HRS and CPB groups). Taken together, these results indicated that HRS may alleviate CPB-induced myocardial injury, inhibit myocardial cell apoptosis and protect myocardial cells through regulation of the JAK2/STAT3 signaling pathway.

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Hydrogen-Rich Saline Attenuates Lipopolysaccharide-Induced Heart Dysfunction by Restoring Fatty Acid Oxidation in Rats by Mitigating c-Jun n-Terminal Kinase Activation

Cited by 15 publications

References 0 publications

Inhalation of Hydrogen Attenuates Progression of Chronic Heart Failure via Suppression of Oxidative Stress and P53 Related to Apoptosis Pathway in Rats

Inhalation of Hydrogen Attenuates Progression of Chronic Heart Failure via Suppression of Oxidative Stress and P53 Related to Apoptosis Pathway in Rats

Hydrogen Flush After Cold Storage as a New End‐Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury

Hydrogen‑rich solution attenuates myocardial injury caused by cardiopulmonary bypass in rats via the Janus‑activated kinase 2/signal transducer and activator of transcription 3 signaling pathway

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