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We are analyzing https://link.springer.com/article/10.1186/s12872-018-0773-9.

Title:
Protective effect of hydrogen-rich saline on pressure overload-induced cardiac hypertrophyin rats: possible role of JAK-STAT signaling | BMC Cardiovascular Disorders
Description:
Background Molecular hydrogen has been shown to have antioxidant effect and have been used to prevent oxidative stress-related diseases. The goal of this study was to explore if hydrogen-rich saline (HRS) plays a cardioprotective effect on abdominal aortic constriction (AAC) induced cardiac hypertrophy in rats. 60adult Sprague–Dawley rats received surgically the AAC for 6-week. After the surgery, the rats were randomly divided into 4 groups (15 for each):1: sham-operated (sham); 2: AAC-model; 3: AAC + Low HRS (LHRS); and 4: AAC + High HRS (HHRS). The rats in sham and AAC-model groups were treated with normal saline intraperitoneally, while rats in LHRS and HHRS groups were intraperitoneally treated with 3 or 6 mL/kg HRS daily, respectively, for 6-week. Results The ratios of HW/BW and LVW/BW were shown in an order of Model > LHRS > HHRS > SHAM groups. The cardiac hypertrophy was also manifested with increased expressions of atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP) and fibrosis of cardiac tissues in AAC-model group, which could likewise be restrained in LHRS and HHRS groups. Moreover, the JAK-STAT (Janus Kinase-Signal transducers and activators of transcription) signaling molecule expressions were decreased with HRS treatment. Conclusions Our results showed a protective effect of HRS on pressure overload-induced cardiac hypertrophy in rats, which may be associated to a decreasing in JAK-STAT signaling pathway.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

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Topics {✒️}

l-arginine-induced acute pancreatitis c-raf/erk1/2 signaling pathway high-dose chemotherapy-induced cardiotoxicity hydrogen-rich saline ameliorates neonatal brain hypoxia-ischemia article download pdf jak-stat signaling pathway angiotensin-converting enzyme inhibition janus kinase-signal transducers dutp nick-end labeling janus kinase/signal transducer myocardial ischemia/reperfusion injury myocardial ischemia-reperfusion injury natural day/night cycle pressure overload induced cardiac hypertrophy induced induced cardiac hypertrophy 6 ml/kg hrs daily hypertensive cardiovascular events hydrogen-rich saline sham-operated rats received lv working disorders technology research project oxidative stress markers aac-model group showed organ injury caused p-stat3 protein level left ventricular hypertrophy jak-stat pathway jak/stat pathway jak-stat signaling cardiac hypertrophy model full access pathological cardiac hypertrophy cardiac hypertrophy due privacy choices/manage cookies p-stat3 expression levels intestinal ischemia/reperfusion left ventricular tissues ventricular hypertrophy 6 weeks prevent cardiac hypertrophy creative commons license left ventricular weight reduce blood pressure european economic area attenuating oxidative stress reducing oxidative stress aac-treated rat hearts 6 ml/kg reduced brain natriuretic peptides

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Protective effect of hydrogen-rich saline on pressure overload-induced cardiac hypertrophyin rats: possible role of JAK-STAT signaling
         description:Molecular hydrogen has been shown to have antioxidant effect and have been used to prevent oxidative stress-related diseases. The goal of this study was to explore if hydrogen-rich saline (HRS) plays a cardioprotective effect on abdominal aortic constriction (AAC) induced cardiac hypertrophy in rats. 60adult Sprague–Dawley rats received surgically the AAC for 6-week. After the surgery, the rats were randomly divided into 4 groups (15 for each):1: sham-operated (sham); 2: AAC-model; 3: AAC + Low HRS (LHRS); and 4: AAC + High HRS (HHRS). The rats in sham and AAC-model groups were treated with normal saline intraperitoneally, while rats in LHRS and HHRS groups were intraperitoneally treated with 3 or 6 mL/kg HRS daily, respectively, for 6-week. The ratios of HW/BW and LVW/BW were shown in an order of Model > LHRS > HHRS > SHAM groups. The cardiac hypertrophy was also manifested with increased expressions of atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP) and fibrosis of cardiac tissues in AAC-model group, which could likewise be restrained in LHRS and HHRS groups. Moreover, the JAK-STAT (Janus Kinase-Signal transducers and activators of transcription) signaling molecule expressions were decreased with HRS treatment. Our results showed a protective effect of HRS on pressure overload-induced cardiac hypertrophy in rats, which may be associated to a decreasing in JAK-STAT signaling pathway.
         datePublished:2018-02-13T00:00:00Z
         dateModified:2018-02-13T00:00:00Z
         pageStart:1
         pageEnd:7
         license:http://creativecommons.org/publicdomain/zero/1.0/
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            HRS
            Cardiac hypertrophy
            Signaling pathway
            Cardiology
            Cardiac Surgery
            Angiology
            Blood Transfusion Medicine
            Internal Medicine
            Medicine/Public Health
            general
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      headline:Protective effect of hydrogen-rich saline on pressure overload-induced cardiac hypertrophyin rats: possible role of JAK-STAT signaling
      description:Molecular hydrogen has been shown to have antioxidant effect and have been used to prevent oxidative stress-related diseases. The goal of this study was to explore if hydrogen-rich saline (HRS) plays a cardioprotective effect on abdominal aortic constriction (AAC) induced cardiac hypertrophy in rats. 60adult Sprague–Dawley rats received surgically the AAC for 6-week. After the surgery, the rats were randomly divided into 4 groups (15 for each):1: sham-operated (sham); 2: AAC-model; 3: AAC + Low HRS (LHRS); and 4: AAC + High HRS (HHRS). The rats in sham and AAC-model groups were treated with normal saline intraperitoneally, while rats in LHRS and HHRS groups were intraperitoneally treated with 3 or 6 mL/kg HRS daily, respectively, for 6-week. The ratios of HW/BW and LVW/BW were shown in an order of Model > LHRS > HHRS > SHAM groups. The cardiac hypertrophy was also manifested with increased expressions of atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP) and fibrosis of cardiac tissues in AAC-model group, which could likewise be restrained in LHRS and HHRS groups. Moreover, the JAK-STAT (Janus Kinase-Signal transducers and activators of transcription) signaling molecule expressions were decreased with HRS treatment. Our results showed a protective effect of HRS on pressure overload-induced cardiac hypertrophy in rats, which may be associated to a decreasing in JAK-STAT signaling pathway.
      datePublished:2018-02-13T00:00:00Z
      dateModified:2018-02-13T00:00:00Z
      pageStart:1
      pageEnd:7
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12872-018-0773-9
      keywords:
         HRS
         Cardiac hypertrophy
         Signaling pathway
         Cardiology
         Cardiac Surgery
         Angiology
         Blood Transfusion Medicine
         Internal Medicine
         Medicine/Public Health
         general
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs12872-018-0773-9/MediaObjects/12872_2018_773_Fig1_HTML.gif
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                     type:PostalAddress
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                     type:PostalAddress
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                     type:PostalAddress
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                  address:
                     name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
                     type:PostalAddress
                  type:Organization
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            name:Lu Fu
            url:http://orcid.org/0000-0001-5953-1891
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            address:
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      name:Zhiwei Huang
      affiliation:
            name:First Affiliated Hospital of Harbin Medical University
            address:
               name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
               type:PostalAddress
            type:Organization
      name:Fenghua Xue
      affiliation:
            name:First Affiliated Hospital of Harbin Medical University
            address:
               name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
               type:PostalAddress
            type:Organization
      name:Shujing Wu
      affiliation:
            name:First Affiliated Hospital of Harbin Medical University
            address:
               name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
               type:PostalAddress
            type:Organization
      name:Jing Yang
      affiliation:
            name:First Affiliated Hospital of Harbin Medical University
            address:
               name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
               type:PostalAddress
            type:Organization
      name:Liqun Zhu
      affiliation:
            name:First Affiliated Hospital of Harbin Medical University
            address:
               name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
               type:PostalAddress
            type:Organization
      name:Lu Fu
      url:http://orcid.org/0000-0001-5953-1891
      affiliation:
            name:First Affiliated Hospital of Harbin Medical University
            address:
               name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Emergency Department, Heilongjiang Provincial Hospital, Harbin, China
      name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China
      name:Department of Cardiovascular Medicine, First Affiliated Hospital of Harbin Medical University, Harbin, China

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