羟基红花黄色素A抗心肌缺血-再灌注损伤作用与钙超载相关性研究
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摘要
目的通过外科手术方法建立大鼠心肌缺血再灌注损伤模型,探讨羟基红花黄色素A(HSYA)抗心肌缺血-再灌注损伤作用与钙超载相关性.方法采用培养的SD大鼠心肌细胞缺氧再灌注损伤模型,实验分为5组:假手术组(Sham,1),缺血-再灌注1 h组(1 h,2),缺血-再灌注24 h组(24 h,3),缺血-再灌注1 h+HSYA组(1 h+,4),缺血-再灌注24 h+HSYA组(24 h+,5).比较缺血-再灌注大鼠心肌细胞内钙离子浓度的变化,并进行心肌细胞膜钙ATP酶MCA和SERCA的表达检测.结果与正常对照组(Sham)比较,缺血-再灌注组(1 h,24 h)细胞内钙离子浓度明显升高,且以再灌注24 h更明显(P<0.05);与再灌注组(1 h,24 h)比较,HSYA治疗后组(1 h+,24h+)钙离子浓度明显降低(P<0.05);1 h+和24 h+组肌浆网钙离子ATP酶SERCA表达与Sham组比较显著降低(P<0.05),而与1 h和24 h组比较显著升高(P<0.01).结论心肌缺血-再灌注损伤与钙超载有关,HSYA抗心肌缺血-再灌注引起的钙超载由SERCA调控,而非PMCA调控.
Objective To explore the relationship between effect of HSYA on myocardial ischemia-reperfusion injury and calcium overload by establishing myocardial ischemia-reperfusion injury rat model through surgical method. Method Myocardial cell hypoxia reperfusion damage model of the cultured SD rats was employed to conduct the experiment,which was divided into five groups: the control group( Sham,1),ischemia-reperfusion group for 1 hour( 1 h,2),ischemia-reperfusion group for 24 hours( 24 h,3),ischemia-reperfusion group for 1 hour treated with HSYA( 1 h +,4),ischemia-reperfusion group for 24 hours treated with HSYA( 24 h +,5).Changes of calcium ion concentration in the cardiomyocytes of ischemia-reperfusion rats were compared,and the expression of myocardial cell membrane ATPase MCA and SERCA were detected. Results Compared with the normal control group( Sham),intracellular calcium ion concentration increased significantly in ischemia-reperfusion group( 1 h,24 h),and the phenomenon was more obvious for 24 h reperfusion( P<0. 05). Compared with the reperfusion group( 1 h,24 h),calcium ion concentration decreased significantly in HSYA group after treatment( 1 h +,24 h +)( P<0. 05). The expressions of sarcoplasmic reticulum calcium ATPase SERCA in 1 + h and 24 h + groups decreased significantly compared with the Sham group( P<0. 05),but they significantly increased compared with 1 h and 24 h groups( P < 0. 01). Conclusion Myocardial ischemia-reperfusion injury was associated with calcium overload,and calcium overload was caused by myocardial ischemia-reperfusion resulting from the effect of HSYA which was regulated by SERCA,rather than PMCA.
Objective To explore the relationship between effect of HSYA on myocardial ischemia-reperfusion injury and calcium overload by establishing myocardial ischemia-reperfusion injury rat model through surgical method. Method Myocardial cell hypoxia reperfusion damage model of the cultured SD rats was employed to conduct the experiment,which was divided into five groups: the control group( Sham,1),ischemia-reperfusion group for 1 hour( 1 h,2),ischemia-reperfusion group for 24 hours( 24 h,3),ischemia-reperfusion group for 1 hour treated with HSYA( 1 h +,4),ischemia-reperfusion group for 24 hours treated with HSYA( 24 h +,5).Changes of calcium ion concentration in the cardiomyocytes of ischemia-reperfusion rats were compared,and the expression of myocardial cell membrane ATPase MCA and SERCA were detected. Results Compared with the normal control group( Sham),intracellular calcium ion concentration increased significantly in ischemia-reperfusion group( 1 h,24 h),and the phenomenon was more obvious for 24 h reperfusion( P<0. 05). Compared with the reperfusion group( 1 h,24 h),calcium ion concentration decreased significantly in HSYA group after treatment( 1 h +,24 h +)( P<0. 05). The expressions of sarcoplasmic reticulum calcium ATPase SERCA in 1 + h and 24 h + groups decreased significantly compared with the Sham group( P<0. 05),but they significantly increased compared with 1 h and 24 h groups( P < 0. 01). Conclusion Myocardial ischemia-reperfusion injury was associated with calcium overload,and calcium overload was caused by myocardial ischemia-reperfusion resulting from the effect of HSYA which was regulated by SERCA,rather than PMCA.
引文
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[10]田兰,吴桂荣,王岩.红花黄色素研究进展[J].西北药学杂志,2007,22(4):218-220.
[11]Haworth R A,Potter K T,Russell D C.Role of arachidonic acid,lipoxygenase,and mitochondrial depolarization in reperfusion arrhythmias[J].Am J Physiol Heart Circ Physiol,2010,299(1):165-174.
[2]郭来敬,张志仁,陈东辉,等.电子顺磁共振检测心肌缺血再灌产生的氧自由基及其保护作用的实验研究[J].心肺血管病杂志,2000,19(1):58-60.
[3]谷天祥,张显清,谷春久,等.心肌缺血再灌注亚细胞钙变化电镜细胞化学研究[J].中国医科大学学报,1996,25(3):270-273.
[4]张芸,张芙荣,陈君柱,等.HOF642对心肌缺血再灌注损伤及细胞凋亡的影响[J].中国病理生理杂志,2002,18(1):36-39.
[5]郏俊华.生药学[M].3版.北京:人民卫生出版社,1999:263-265.
[6]Romano C,Price M,Bai H Y,et al.Neuroprotectants in Honghua:glucose attenuates retinal ischemic damage[J].Invest Ophthalmol Vis Sci,1993,34:72-80.
[7]蔡广,陈国璋.红花黄色素的临床应用进展[J].华南国防医学杂志,2003,17(1):13-15.
[8]Y e S Y,Gao W Y.Hydroxysafflor yellow A protects neuron again thypoxia injury and suppresses inflammatory responses following focal ischemia reperfusion in rats[J].Arch Pharm Res,2008,31(8):1010-1015.
[9]罗涛,岳荣川,胡厚祥.心肌缺血-再灌注损伤钙超载及其防治策略[J].国际心血管病杂志,2011,38(1):21-24.
[10]田兰,吴桂荣,王岩.红花黄色素研究进展[J].西北药学杂志,2007,22(4):218-220.
[11]Haworth R A,Potter K T,Russell D C.Role of arachidonic acid,lipoxygenase,and mitochondrial depolarization in reperfusion arrhythmias[J].Am J Physiol Heart Circ Physiol,2010,299(1):165-174.