Chronic hydrogen-rich saline treatment reduces oxidative stress and attenuates left ventricular hypertrophy in spontaneous hypertensive rats

Yu, Yongsheng; Zheng, Hao

doi:10.1007/s11010-012-1264-4

Cited by 41 publications

(31 citation statements)

References 38 publications

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“…Based on previous studies and our data, the possible mechanism of H2 on the therapy of AA might be as follows. Firstly, it was reported that H2 inhibited NF-▩B activation, which causes a transcriptional up-regulation of inflammatory cytokines, such as TNF-α, IL-6, IFN-γ etc [24,34,35]. These cytokines was also found decreased in the H2 treated groups in our experiment, indicating NF-▩B as a possible target for the regulating effect of H2 on the cytokines microenvironment.…”

Section: Discussionsupporting

confidence: 57%

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Therapeutic Effects of Hydrogen-Rich Solution on Aplastic Anemia in Vivo

Zhao

Mei

Qian

et al. 2013

Cell Physiol Biochem

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Background: Aplasitc anemia (AA) is a bone marrow failure syndrome characterized by an immune-mediated destruction of hematopoietic stem cells. Though clinical symptoms could be ameliorated by bone marrow transplantation and/or immunosuppressive therapy, frequent recurrence and especially evolution of clonal hematologic diseases remains problematic clinically. Cytokines such as interferon-γ (INF-γ), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) secreted by autologous T cells are closely related with the development of AA. Hydrogen-rich solution was reported to inhibit the levels of cytokines including INF-γ, TNF-α and IL-6 in vivo in recent studies. This study was to investigate the potential therapeutic effects of hydrogen-rich solution on AA in vivo. Methods: AA model was determined in vivo by mice and body weights of the mice were used as the basic physiological index. Peripheral blood cells were calculated to evaluate the hematologic recovery degree. Bone marrow nucleated cells (BMNCs), tissue histology, as well as CFU-S and CFU-GM forming units were used to evaluate the recovery of bone marrow microenvironment. The ratio of CD4⁺ and CD8⁺ cells were examined along with cytokine levels in serum to determine the efficacy of H₂-rich solution on the affected immunological functions. Results: Body weight and number of peripheral blood cells were significantly improved for mice in the H₂-rich solution treated groups as compared with those with AA. The number of BMNCs and CFUs increased markedly and the bone marrow microenvironment was also improved significantly. The experimental group restrained the cell apoptosis, relieved hyperemia and accelerated tissue repair. The number of CD4⁺ and CD8⁺ cells as well as the ratio of CD4/CD8 increased to normal gradually, while the levels of TNF-α, IFN-γ, and IL-6 in serum decreased after H₂-rich solution treatment. Conclusion: Our study firstly showed that hydrogen-rich solution accelerated the recovery of either hematological or immunological recovery on aplastic anemia mice. This finding suggests hydrogen-rich solution as a potential clinical therapeutic agent for AA.

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Section: Discussionsupporting

confidence: 57%

“…Meanwhile, our research determined that hydrogen can protect mice from GVHD by regulating TNF-α, IL-2, IL-10 [17]. Hydrogen was also demonstrated to be able to down-regulate levels of various cytokines, including TNF-α, IFN-γ, IL-1, IL-6, IL-12 in different models [24,25,26]. These cytokines play important roles in AA.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Effects of Hydrogen-Rich Solution on Aplastic Anemia in Vivo

Zhao

Mei

Qian

et al. 2013

Cell Physiol Biochem

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“…Drinking H 2 -rich water blocks cardiac fibrosis induced by left kidney artery ischemia/reperfusion injury (Zhu et al, 2011). H 2 -rich saline injection also inhibits ischemia/reperfusion (Sun et al, 2009), or hypertension-mediated cardiac remodeling (Wang et al, 2011; Yu and Zheng, 2012). However, the effects of intraperitoneal injection of H 2 on cardiac hypertrophy induced by β-adrenoceptor stimulation have not yet been clarified.…”

Section: Discussionmentioning

confidence: 99%

“…These findings confirm that the anti-hypertrophic effect of H 2 is partially achieved through blocking ROS-dependent MAPKs signaling. Yu Yongsheng et al has reported that H 2 -rich saline inhibits cardiac hypertrophy in spontaneous hypertensive rats (SHRs) via blocking NF-κB activity (Yu and Zheng, 2012). H 2 -rich saline reduces myocardial reperfusion injury and improves heart function through down-regulating the expression of Akt and GSK3β (Yue et al, 2015), and blocking autophagy in myocardial tissue (Pan et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen (H2) Inhibits Isoproterenol-Induced Cardiac Hypertrophy via Antioxidative Pathways

Zhang

Long

et al. 2016

Front. Pharmacol.

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Background and Purpose: Hydrogen (H2) has been shown to have a strong antioxidant effect on preventing oxidative stress-related diseases. The goal of the present study is to determine the pharmacodynamics of H2 in a model of isoproterenol (ISO)-induced cardiac hypertrophy.Methods: Mice (C57BL/6J; 8–10 weeks of age) were randomly assigned to four groups: Control group (n = 10), ISO group (n = 12), ISO plus H2 group (n = 12), and H2 group (n = 12). Mice received H2 (1 ml/100g/day, intraperitoneal injection) for 7 days before ISO (0.5 mg/100g/day, subcutaneous injection) infusion, and then received ISO with or without H2 for another 7 days. Then, cardiac function was evaluated by echocardiography. Cardiac hypertrophy was reflected by heart weight/body weight, gross morphology of hearts, and heart sections stained with hematoxylin and eosin, and relative atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) mRNA levels. Cardiac reactive oxygen species (ROS), 3-nitrotyrosine and p67 (phox) levels were analyzed by dihydroethidium staining, immunohistochemistry and Western blotting, respectively. For in vitro study, H9c2 cardiomyocytes were pretreated with H2-rich medium for 30 min, and then treated with ISO (10 μM) for the indicated time. The medium and ISO were re-changed every 24 h. Cardiomyocyte surface areas, relative ANP and BNP mRNA levels, the expression of 3-nitrotyrosine, and the dissipation of mitochondrial membrane potential (MMP) were examined. Moreover, the expression of extracellular signal-regulated kinase1/2 (ERK1/2), p-ERK1/2, p38, p-p38, c-Jun NH2-terminal kinase (JNK), and p-JNK were measured by Western blotting both in vivo and in vitro.Results: Intraperitoneal injection of H2 prevented cardiac hypertrophy and improved cardiac function in ISO-infused mice. H2-rich medium blocked ISO-mediated cardiomyocytes hypertrophy in vitro. H2 blocked the excessive expression of NADPH oxidase and the accumulation of ROS, attenuated the decrease of MMP, and inhibited ROS-sensitive ERK1/2, p38, and JNK signaling pathways.Conclusion: H2 inhibits ISO-induced cardiac/cardiomyocytes hypertrophy both in vivo and in vitro, and improves the impaired left ventricular function. H2 exerts its protective effects partially through blocking ROS-sensitive ERK1/2, p38, and JNK signaling pathways.

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“…The protective effects of H 2 on cardiac hypertrophy were also confirmed in SHR. H 2 -rich saline attenuates left ventricular hypertrophy in SHR via suppressing inflammatory process, abating oxidative stress, preserving mitochondrial function, and inhibition of Ang II levels in left ventricles locally might also be involved [51]. …”

Section: The Effects Of H2 In Heart Diseasesmentioning

confidence: 99%

Hydrogen Therapy in Cardiovascular and Metabolic Diseases: from Bench to Bedside

Zhang

Tan

et al. 2018

Cell Physiol Biochem

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Hydrogen (H₂) is colorless, odorless, and the lightest of gas molecules. Studies in the past ten years have indicated that H₂ is extremely important in regulating the homeostasis of the cardiovascular system and metabolic activity. Delivery of H₂ by various strategies improves cardiometabolic diseases, including atherosclerosis, vascular injury, ischemic or hypertrophic ventricular remodeling, intermittent hypoxia- or heart transplantation-induced heart injury, obesity and diabetes in animal models or in clinical trials. The purpose of this review is to summarize the physical and chemical properties of H₂, and then, the functions of H₂ with an emphasis on the therapeutic potential and molecular mechanisms involved in the diseases above. We hope this review will provide the future outlook of H₂-based therapies for cardiometabolic disease.

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Chronic hydrogen-rich saline treatment reduces oxidative stress and attenuates left ventricular hypertrophy in spontaneous hypertensive rats

Cited by 41 publications

References 38 publications

Therapeutic Effects of Hydrogen-Rich Solution on Aplastic Anemia in Vivo

Therapeutic Effects of Hydrogen-Rich Solution on Aplastic Anemia in Vivo

Hydrogen (H2) Inhibits Isoproterenol-Induced Cardiac Hypertrophy via Antioxidative Pathways

Hydrogen Therapy in Cardiovascular and Metabolic Diseases: from Bench to Bedside

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