Xia Rui, Zhao Bo, Wu Yang, Hou Jia-Bao, Zhang Li, Xu Jin-Jin, Xia Zhong-Yuan
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
J Biomed Biotechnol. 2011;2011:767930. doi: 10.1155/2011/767930. Epub 2011 Oct 16.
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.
糖尿病与心肌中一氧化氮（NO）生物利用度降低有关。人参皂苷Rb1已被证明对缺血再灌注损伤具有心脏保护作用。本研究的目的是探讨人参皂苷Rb1在糖尿病大鼠心肌缺血再灌注期间是否发挥心脏保护作用，以及这种作用是否与通过增强心肌中内皮型一氧化氮合酶（eNOS）表达来增加NO的产生有关。通过阻断左冠状动脉前降支30分钟，然后再灌注120分钟来诱导心肌缺血/再灌注（I/R）损伤。在诱导缺血前25分钟或10分钟分别给予eNOS抑制剂L-NAME或Rb1。与人参皂苷Rb1预处理组相比，I/R组心肌梗死面积减小。人参皂苷Rb1诱导的心肌保护作用伴随着eNOS表达增加、NO浓度升高以及血浆肌酸激酶（CK）和乳酸脱氢酶（LDH）降低（P<0.05）。此外，人参皂苷Rb1减轻了心肌氧化应激和组织学损伤（P<0.05）。L-NAME消除了人参皂苷Rb1的保护作用。结论是人参皂苷Rb1通过增强eNOS表达、增加NO含量以及抑制氧化应激来保护糖尿病大鼠免受心肌缺血/再灌注损伤。
