Ginsenoside Rb1 preconditioning enhances eNOS expression and attenuates myocardial ischemia/reperfusion injury in diabetic rats.

Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ische...

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Publicado en:Journal of Biomedicine & Biotechnology pp. 767930 - 767931
Autores principales: Xia, Rui, Zhao, Bo, Wu, Yang, Hou, Jia-Bao, Zhang, Li, Xu, Jin-Jin, Xia, Zhong-Yuan
Formato: research Journal Article
Publicado: Wiley-Blackwell 2011
Acceso en línea:Ver este registro en EBSCOhost
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      pub: Wiley-Blackwell
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        atl: Ginsenoside Rb1 preconditioning enhances eNOS expression and attenuates myocardial ischemia/reperfusion injury in diabetic rats.
      aug:
        au:
          Xia, Rui
          Zhao, Bo
          Wu, Yang
          Hou, Jia-Bao
          Zhang, Li
          Xu, Jin-Jin
          Xia, Zhong-Yuan
        affil: Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
      sug:
        subj:
          Diabetes Mellitus
          Glycosides Pharmacodynamics
          Myocardial Ischemia
          Myocardial Reperfusion Injury
          Myocardium
          Nitric Oxide Metabolism
          Oxidoreductases
          Animals
          Apoptosis Drug Effects
          Creatine Kinase Blood
          Gene Expression Drug Effects
          Lactate Dehydrogenase Blood
          Male
          Myocardium Pathology
          Arginine Pharmacodynamics
          Oxidative Stress Drug Effects
          Rats
          Male
      ab: Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (P < 0.05). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (P < 0.05). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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