摘要
目的探讨青蒿素是否可以通过调节自噬减轻心肌缺血再灌注(I/R)损伤以及可能的机制。方法采用大鼠心肌I/R模型(缺血30min,再灌注4h),雄性SD大鼠30只随机分为3组:假手术组(SO组,n=10)、缺血再灌注组(I/R组,n=10)和青蒿素治疗组(A+I/R组,n=10,Arteannuin:25mg/kg,Tid,造模前1d灌胃)。检测心肌损伤标记物肌酸激酶(CK)、乳酸脱氢酶(LDH)和肌钙蛋白I(c Tn I);检测氧化应激水平(丙二醛(MDA)和超氧化物歧化酶(SOD)水平;检测自噬蛋白beclin-1和LC3水平。结果与SO组比较,I/R组可诱导心肌损伤标记物,氧化应激水平的增加和自噬的过度激活;与I/R组比较,青蒿素可显著的降低心肌损伤标记物的表达、氧化应激水平和自噬的过度激活。结论 1青蒿素可以通过抑制过度自噬减轻心肌I/R损伤;2青蒿素可能通过抑制氧化应激,抑制再灌注阶段自噬过度激活。
Objective To investigate the protective effect of artemisinin on myocardial ischemia and repeifusion( I/ R ) injury and the possible mechanism. Methods Rat I/R model was established by ligation of left anterior descending coronary artery for3 0 m in, followed by repeifusion for 4 h . 30 rats were divided into three groups: sham-operated group ( S O ) , ischemia and reperfusion group ( I/ R ) and artemisinin treatment group ( A + I/ R ) ,10 rats in each group. Cardiac injury markers (serum creatine ( C K ) , lactate dehydrogenase ( LDH ) ,and cT n l) , oxidative stress indexes ( malondialdehyde (M D A ) and superoxide dismutase ( SO D ) and autophagy markers (beclin-1 and LC3) were detected. Results Compared with SO group,the levels of C K ,LDH ,cTnI MDA and the activity of SOD were significantly increased ; autophagy was excessively activated in I/R group.Compared with I/R group, artemisinin significantly decreased the contents of C K ,LD H ,cTnI and MDA and increased the activity of SOD in myocardial tissue, decreased beclin-1 level and LC3 - II/ I ratio, suppressed excessive activation of autophagy . Conclusion Artemisinin can protect against myocardial I/R injury via suppressing oxidative stress and excessiveof activation autophagy.
作者
沈秀珍
王凌
方毅华
SHEN Xiu-zhen;WAN GLing;FANG Yi-huang(Department of Cardiology,People'Hospital of Chibi, Chibi Hubei 4373QQ,China)
出处
《湖北科技学院学报（医学版）》
2016年第3期191-193,共3页
Journal of Hubei University of Science and Technology(Medical Sciences)
关键词
青蒿素
自噬
氧化应激
心肌缺血
再灌注损伤
Artemisinin
Autophagy
Oxidative stress
Myocardial ischemia
Repeifusion injury
