中国药师
中國藥師
중국약사
CHINA PHARMACIST
2015年
6期
926-928
,共3页
刘文霞%树俊莲%徐丽%曹军平%马毅
劉文霞%樹俊蓮%徐麗%曹軍平%馬毅
류문하%수준련%서려%조군평%마의
芍药苷%心肌缺血再灌注损伤%超氧化物歧化酶%丙二醛
芍藥苷%心肌缺血再灌註損傷%超氧化物歧化酶%丙二醛
작약감%심기결혈재관주손상%초양화물기화매%병이철
Paeoniflorin%Myocardial ischemia/reperfusion injury%SOD%MDA
目的::观察芍药苷对大鼠心肌缺血再灌注( myocardial ischemia/reperfusion, MI/R)损伤的保护作用,探讨其作用机制。方法:结扎冠脉造成心肌缺血30 min再灌注2 h,建立MI/R损伤大鼠模型,随机分为假手术组、模型组、芍药苷三个剂量组(20,10,5 mg·kg-1)(n=10),于术前1 h和再灌注即刻分别进行尾静脉注射给药。取血清,测定肌酸激酶(CK)、乳酸脱氯酶( LDH)、超氧化物歧化酶( SOD)活性及丙二醛( MDA)含量;取心脏,测定心肌梗死面积。结果:芍药苷高、中剂量可明显缩小大鼠心肌梗死面积,与模型组比较差异有统计学意义(P<0.05);芍药苷各剂量组可不同程度降低血清CK和LDH活性(P<0.05或P<0.01),升高SOD活性(P<0.01);芍药苷高、中剂量组降低血清MDA含量,与模型组比较差异有统计学意义(P<0.05)。结论:芍药苷预处理对MI/R损伤的保护作用与其减少自由基的生成、抑制脂质过氧化反应等有关。
目的::觀察芍藥苷對大鼠心肌缺血再灌註( myocardial ischemia/reperfusion, MI/R)損傷的保護作用,探討其作用機製。方法:結扎冠脈造成心肌缺血30 min再灌註2 h,建立MI/R損傷大鼠模型,隨機分為假手術組、模型組、芍藥苷三箇劑量組(20,10,5 mg·kg-1)(n=10),于術前1 h和再灌註即刻分彆進行尾靜脈註射給藥。取血清,測定肌痠激酶(CK)、乳痠脫氯酶( LDH)、超氧化物歧化酶( SOD)活性及丙二醛( MDA)含量;取心髒,測定心肌梗死麵積。結果:芍藥苷高、中劑量可明顯縮小大鼠心肌梗死麵積,與模型組比較差異有統計學意義(P<0.05);芍藥苷各劑量組可不同程度降低血清CK和LDH活性(P<0.05或P<0.01),升高SOD活性(P<0.01);芍藥苷高、中劑量組降低血清MDA含量,與模型組比較差異有統計學意義(P<0.05)。結論:芍藥苷預處理對MI/R損傷的保護作用與其減少自由基的生成、抑製脂質過氧化反應等有關。
목적::관찰작약감대대서심기결혈재관주( myocardial ischemia/reperfusion, MI/R)손상적보호작용,탐토기작용궤제。방법:결찰관맥조성심기결혈30 min재관주2 h,건립MI/R손상대서모형,수궤분위가수술조、모형조、작약감삼개제량조(20,10,5 mg·kg-1)(n=10),우술전1 h화재관주즉각분별진행미정맥주사급약。취혈청,측정기산격매(CK)、유산탈록매( LDH)、초양화물기화매( SOD)활성급병이철( MDA)함량;취심장,측정심기경사면적。결과:작약감고、중제량가명현축소대서심기경사면적,여모형조비교차이유통계학의의(P<0.05);작약감각제량조가불동정도강저혈청CK화LDH활성(P<0.05혹P<0.01),승고SOD활성(P<0.01);작약감고、중제량조강저혈청MDA함량,여모형조비교차이유통계학의의(P<0.05)。결론:작약감예처리대MI/R손상적보호작용여기감소자유기적생성、억제지질과양화반응등유관。
Objective:To investigate the protective effects of paeoniflorin on myocardial ischemia/reperfusion ( MI/R) injury in rats. Methods:The rat model of MI/R injury was prepared by coronary artery ligation for 30 min followed by 2-hour reperfusion. Then the rats were randomly divided into 5 groups:sham group, model group, paeoniflorin group respectively at high, medium and low dose (20, 10 and 5 mg·kg-1, n=10). Paeoniflorin was respectively injected via tail vein 1 h before the operation and at the beginning of the reperfusion. The CK, LDH and SOD activities and MDA contents in serum of rats were examined, and the area of myocardial in-farction was also calculated after the reperfusion. Results:Paeoniflorin (20 and 10 mg·kg-1 ) could significantly reduce the area of myocardial infarction when compared with the model group (P<0. 05). Paeoniflorin could obviously inhibit the CK and LDH activities (P<0. 05 or P<0. 01) and enhance the SOD activity (P<0. 01) in serum of MI/R rats. The MDA content in paeoniflorin groups at high and medium dose was significantly lower than that in the model group (P<0. 05). Conclusion:Paeoniflorin pretreatment shows effectiveness against MI/R injury, which may be associated with the inhibition of lipid peroxidation.