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|本期目录/Table of Contents|

梓醇减轻心肌缺血/再灌注损伤及机制

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2015年第3期
页码:
260-264
栏目:
基础研究
出版日期:
2015-01-11

文章信息/Info

Title:
Cardioprotective effects of catalpol against ischemia/reperfusion insult
作者:
贾元红1; 2; 刘文冲2; 王聃红3; 周 望2; 王颖萍2; 李 榕4; 张海锋1
（第四军医大学：1.教学实验中心，3.生理学教研室，4.西京医院老年病科，陕西 西安 710032；
2.西安市卫生学校，陕西 西安 710054）
Author(s):
JIA Yuan-hong1; 2;  LIU Wen-chong2;  WANG Dan-hong3;  ZHOU Wang2;  WANG Ying-ping2;  LI Rong4;  ZHANG Hai-feng1
(1.Center of Teaching Experiment, 3.Department of Physiology, School of Basic Medical Science, 4.Department of Geriatrics, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China；
2.Xi’an Health School, Xi’an 710054, Shaanxi, China)
关键词:
心肌缺血/再灌注损伤; 氧化应激; 硝基化应激; 大鼠
Keywords:
myocardial ischemia/reperfusion injury;  oxidative stress;  nitrative stress;  rat
分类号:
R282.71
DOI:
-
文献标识码:
A
摘要:
目的:观察梓醇是否可减轻急性心肌缺血/再灌注（MI/R）损伤。方法:建立大鼠MI/R模型，随机给予生理盐水和梓醇预处理，全程检测大鼠的心脏功能。再灌注末检测大鼠心肌梗死(MI)面积、心肌细胞凋亡指数、血清肌酸激酶和乳酸脱氢酶的活性、心肌组织过氧亚硝基阴离子（ONOO-）、一氧化氮（NO）、超氧化物及超氧化物歧化酶（SOD）的含量。结果:梓醇预处理可明显改善心脏功能，减少心肌梗死面积和心肌细胞的凋亡与坏死（均P<0.05）。同时，ONOO-和超氧化物的产生也显著减少（P<0.05）；NO和SOD的含量显著增加（均P<0.05）。缺血前给予ONOO-清除剂尿酸（UA）显著减少ONOO-生成及MI范围（P<0.05），但不能额外增强梓醇降低ONOO-及减小MI范围的效应（MI/R+梓醇+UA组 vs. MI/R+梓醇组）。结论:梓醇可抑制ONOO-形成，从而减轻MI/R损伤，其机制可能与增加NO水平及减少超氧化物生成有关。
Abstract:
AIM:To investigate the cardioprotective effect of catalpol in acute myocardial ischemia/reperfusion (MI/R). METHODS: Adult male rats were subjected to 30 min of myocardial ischemia and 3 h of reperfusion and were treated with saline or catalpol (5 mg/kg, i.p., 5 min before reperfusion). Left ventricle systolic pressure (LVSP) and the maximal first derivative of developed pressure (±LV dP/dtmax) were monitored throughout the experiments. Myocardial infarction size, serum creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, apoptosis index, caspase-3 activity, nitric oxide (NO), superoxide dismutase (SOD), superoxide and peroxynitrite (ONOO-) production were determined at the end of reperfusion. RESULTS: Compared with sham, pretreatment with catalpol significantly improved cardiac functions and reduced myocardial infarction, apoptosis and necrosis of cardiomyocytes after MI/R (all P<0.05). Meanwhile, ONOO- formation was markedly reduced after catalpol treatment (3.01±0.22 vs. 4.66±0.53 pmol/mg protein in vehicle, P<0.05). Catalpol increased NO production and anti-oxidant capacity and reduced MI/R-induced superoxide anion (·O-2) production in I/R hearts. In addition, treatment with the potent ONOO- scavenger uric acid (UA) significantly decreased ONOO- production and protected myocardium against MI/R injury, whereas the same treatment with UA could not further enhance cardioprotective effects of catalpol (P>0.05 vs. catalpol alone). CONCLUSION: Catalpol provides cardioprotection against MI/R insult by attenuating ONOO- formation, which is attributable to the increased NO production and decreased ·O-2 production.

参考文献/References

[1]Zweier JL,Talukder MA.The role of oxidants and free radicals in reperfusion injury[J].Cardiovasc Res,2006,70(2):181-190.
[2]Levrand S,Vannay-Bouchiche C,Pesse B,et al.Peroxynitrite is a major trigger of cardiomyocyte apoptosis in vitro and in vivo[J].Free Radic Biol Med,2006,41(6):886-895.
[3]Li DQ,Bao YM,Zhao JJ,et al.Neuroprotective properties of catalpol in transient global cerebral ischemia in gerbils:dose-response,therapeutic time-window and long-term efficacy[J].Brain Res,2004,1029(2):179-185.
[4]Li Y,Bao Y,Jiang B,et al.Catalpol protects primary cultured astrocytes from in vitro ischemia-induced damage[J].Int J Dev Neurosci,2008,26(3-4):309-317.
[5]Li DQ,Duan YL,Bao YM,et al.Neuroprotection of catalpol in transient global ischemia in gerbils[J].Neurosci Res,2004,50(2):169-177.
[6]Zhang HF,Fan Q,Qian XX,et al.Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion[J].Apoptosis,2004,9(6):777-783.
[7]Tian YY,An LJ,Jiang L,et al.Catalpol protects dopaminergic neurons from LPS-induced neurotoxicity in mesencephalic neuron-glia cultures[J].Life Sci, 2006, 80(3):193-199.
[8]Li DQ,Bao YM,Li Y,et al.Catalpol modulates the expressions of Bcl-2 and Bax and attenuates apoptosis in gerbils after ischemic injury[J].Brain Res,2006,1115(1):179-185.
[9]Liang JH,Li YN,Qi JS,et al.eroxynitrite-induced protein nitration is responsible for renal mitochondrial damage in diabetic rat[J].J Endocrinol Invest,2010,33(3):140-146.
[10]Lopez BL,Liu GL,Christopher TA,et al.Peroxynitrite, the product of nitric oxide and superoxide,causes myocardial injury in the isolated perfused rat heart[J].Coron Artery Dis,1997, 8(3/4):149-153.
[11]Ma XL,Lopez BL,Liu GL,et al.Peroxynitrite aggravates myocardial reperfusion injury in the isolated perfused rat heart[J].Cardiovasc Res,1997,36(2):195-204.
[12]Jiao XY,Gao E,Yuan Y,et al.INO-4885[5,10,15,20-tetra[N-(benzyl-4’-carboxylate)-2-pyridinium]-21H,23H-porphine Iron(III) chloride],a peroxynitrite decomposition catalyst, protects the heart against reperfusion injury in mice[J].J Pharmacol Exp Ther,2009,328(3):777-784.
[13]Falk JA,Aune SE,Kutala VK,et al.Inhibition of peroxynitrite precursors, NO and O2, at the onset of reperfusion improves myocardial recovery[J].Resuscitation,2007,74(3):508-515.

备注/Memo

备注/Memo:
收稿日期：2014-07-14.
基金项目：国家自然科学基金项目资助（81270330，81270401，81300190），陕西省科学技术研究发展计划项目资助（2013KJXX-89）
通讯作者：张海锋，副教授，主要从事缺血性心脏病及高血压发病机制与防治研究Email：hfzhang@fmmu.edu.cn
作者简介：贾元红，讲师Email：keanko8899@163.com
更新日期/Last Update: 2015-02-03