摘要
目的探讨自由基清除剂依达拉奉对大鼠心肌再灌注损伤的保护作用及机制。方法将造模成功的24只Wistar大鼠随机分为对照组、缺血再灌注组(再灌注组)、保护组,每组8只。实验结束后检测各组大鼠血清肌酸激酶同工酶(CK-MB)、谷胱甘肽过氧化物酶(GSH-PX)活性及丙二醛水平;光学显微镜观察心肌形态;采用TUNEL和免疫组织化学法分别检测心肌细胞凋亡及心肌凋亡蛋白Bcl-2、Bax的表达。结果与对照组比较,再灌注组大鼠CK MB、丙二醛水平明显升高,GSH-PX活性明显降低,Bcl-2、Bax、Bax/Bcl-2明显升高(P<0.01);与再灌注组比较,保护组大鼠CK-MB、丙二醛水平明显降低,GSH-PX活性明显升高,Bcl-2明显升高,Bax、Bax/Bcl-2明显降低(P<0.01)。与保护组比较,再灌注组大鼠可见大面积心肌梗死,凋亡细胞数明显增加(P<0.01)。结论依达拉奉能够减轻大鼠心肌损伤程度,其机制与减少自由基损伤、抑制心肌细胞凋亡有关。
Objective To investigate the protective effect and mechanism of edaravone against myocardium reperfusion injury in rats.Methods Twenty-four Wistar rats were randomly divided into control group,ischemia-reperfusion group and protective group.After experiment,the activity of CK-MB,GSHPX and concentration of MDA were detected.The myocardial morphology was observed with light microscope.TUNEL staining and immunohistochemical methods were used to determine apoptosis of myocardial cells and expression of Bcl-2 and Bax proteins.Results The activity of serum CK-MB and MDA were higher and the activity of GSHPX was lower in ischemiareperfusion group than in control group.The activity of serum CK-MB and content of MDA were lower and the activity of GSHPX was higher in protective group than in ischemiareperfusion group.There was large area of myocardial infarction in ischemiareperfusion group;but the myocardial injury was lighter in protective group.Apoptotic cells was less in protective group than in ischemiareperfusion group.Bcl-2,Bax protein and the ratio of Bax/Bcl-2 were significantly higher in ischemiareperfusion group than in control group（P〈0.01）,the expression of protein Bcl-2 was significantly higher in protective group than in ischemiareperfusion group（P〈0.01）,but the expression of protein Bax and ratio of Bax/Bcl-2 were significantly lower in protective group than in ischemiareperfusion group,and was higher in ischemiareperfusion group than in control group.Conclusions Edaravone can reduce the extent of myocardial injury,the mechanism is concerned with reducing free radical damage and inhibiting myocardial cell apoptosis.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2010年第8期729-732,共4页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
哈尔滨市青年基金(2003AFQXJ039)
