西安交通大学学报（医学版）
西安交通大學學報（醫學版）
서안교통대학학보（의학판）
JOURNAL OF XI'AN JIAOTONG UNIVERSITY(MEDICAL SCIENCES)
2009年
6期
712-715
,共4页
黄芪%心肌%缺血再灌注损伤
黃芪%心肌%缺血再灌註損傷
황기%심기%결혈재관주손상
Huangqi%myocardium%ischemia-reperfusion injury
目的 探讨黄芪对大鼠缺血再灌注心肌的保护作用及其机制.方法 采用结扎左冠状动脉的方法制备心肌缺血再灌注损伤动物模型.SD大鼠30只随机分为3组:对照组、缺血再灌注组(I/R)和黄芪预处理组(H+I/R).光镜和透射电镜下观察心肌病理变化,检测血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,以及心肌组织Na~+K~+-ATP酶(Na~+K~+-ATPase)、Ca~(2+)-ATP酶(Ca~(2+)-ATPase)活性.结果 ①黄芪预处理组光镜和透射电镜下心肌细胞变性坏死程度及心肌细胞超微结构形态改变较缺血再灌注组显著减轻;②黄芪预处理组大鼠血清中CK、LDH活性和MDA含量显著降低(P<0.05),SOD、Na+ K+-ATPase、Ca~(2+)-ATPase活性显著提高(P<0.05).结论 黄芪对大鼠冠状动脉结扎后再灌注心肌损伤具有明显的保护作用,其机制可能与改善心肌缺血再灌注冠状微循环与抗氧自由基生成、减轻钙超载等多种机制有关.
目的 探討黃芪對大鼠缺血再灌註心肌的保護作用及其機製.方法 採用結扎左冠狀動脈的方法製備心肌缺血再灌註損傷動物模型.SD大鼠30隻隨機分為3組:對照組、缺血再灌註組(I/R)和黃芪預處理組(H+I/R).光鏡和透射電鏡下觀察心肌病理變化,檢測血清肌痠激酶(CK)、乳痠脫氫酶(LDH)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,以及心肌組織Na~+K~+-ATP酶(Na~+K~+-ATPase)、Ca~(2+)-ATP酶(Ca~(2+)-ATPase)活性.結果 ①黃芪預處理組光鏡和透射電鏡下心肌細胞變性壞死程度及心肌細胞超微結構形態改變較缺血再灌註組顯著減輕;②黃芪預處理組大鼠血清中CK、LDH活性和MDA含量顯著降低(P<0.05),SOD、Na+ K+-ATPase、Ca~(2+)-ATPase活性顯著提高(P<0.05).結論 黃芪對大鼠冠狀動脈結扎後再灌註心肌損傷具有明顯的保護作用,其機製可能與改善心肌缺血再灌註冠狀微循環與抗氧自由基生成、減輕鈣超載等多種機製有關.
목적 탐토황기대대서결혈재관주심기적보호작용급기궤제.방법 채용결찰좌관상동맥적방법제비심기결혈재관주손상동물모형.SD대서30지수궤분위3조:대조조、결혈재관주조(I/R)화황기예처리조(H+I/R).광경화투사전경하관찰심기병리변화,검측혈청기산격매(CK)、유산탈경매(LDH)、초양화물기화매(SOD)활성화병이철(MDA)함량,이급심기조직Na~+K~+-ATP매(Na~+K~+-ATPase)、Ca~(2+)-ATP매(Ca~(2+)-ATPase)활성.결과 ①황기예처리조광경화투사전경하심기세포변성배사정도급심기세포초미결구형태개변교결혈재관주조현저감경;②황기예처리조대서혈청중CK、LDH활성화MDA함량현저강저(P<0.05),SOD、Na+ K+-ATPase、Ca~(2+)-ATPase활성현저제고(P<0.05).결론 황기대대서관상동맥결찰후재관주심기손상구유명현적보호작용,기궤제가능여개선심기결혈재관주관상미순배여항양자유기생성、감경개초재등다충궤제유관.
Objective To study the effects and mechanism of Huangqi against myocardium injury induced by ischemia and reperfusion in rats. Methods Totally 30 male Sprague-Dauley rats were randomly divided into three groups: control group (C group), ischemia/reperfusion group (I/R group), ischemic pretreatment with Huangqi group (H+I/R group), with 10 rats in each. The left anterior descending (LAD) coronary artery was ligated to establish the ischemia/reperfusion heart model. Huangqi was administered before the model was established in the H+I/R group. The pathologic changes of myocardial tissues (under light and electron microscopy), content of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in serum, as well as activities of Na~+K~+-ATPase and Ca~(2+)-ATPase in myocardial tissues were observed. Results Light and electron microscopic examination showed that the necrotic degeneration and pathologic changes of myocardiocytes in Huangqi group were significantly milder than those in the model group. The levels of CK, LDH, MDA were decreased significantly in Huangqi group (P<0.05), the activities of SOD, Na~+K~+-ATPase and Ca~(2+)-ATPase in myocardial tissues in Huangqi group significantly increased (P<0.05). Conclusion Huangqi shows a significantly protective effect on myocardial I/R injury in rats. The mechanism may be related to multiple factors, including improving microcirculation, forming anti-oxygen free radicals and decreasing calcium overload.
