CrkL在β受体过度激动促进心肌梗死后心室间质重塑中的作用

The role of CrkL in the effect of extracellular matrix remodeling of left ventricle of post-myocardial infarction rats by β-adrenergic receptor over-actuation treatment

目的探讨CrkL在β肾上腺素能受体(β-AR)过度激动促进心肌梗死后心室间质重塑中的作用。方法40只SD大鼠分为心肌梗死给药组(n=15);心肌梗死对照组(n=10);假手术给药组(n=9)以及假手术对照组(n=6),采用左冠状动脉前降支结扎术建立心肌梗死模型,心肌梗死给药组和假手术给药组给予异丙肾上腺素,心肌梗死对照组和假手术对照组给予生理盐水处理,采用彩色多普勒超声测定射血分数(EF)及左室短轴缩短率(FS),12w后处死大鼠,取心脏,Masson胶原特殊染色法测定胶原容积分数(CVF),Western印迹检测心肌梗死周围濒死组织CrkL的表达。结果心肌梗死给药组较心肌梗死对照组EF及FS降低、CVF增高、梗死灶周围濒死组织中CrkL蛋白表达显著升高并与CVF呈正相关(P<0.05)。结论β-AR过度激动可明显增强心肌梗死后心室间质重塑,CrkL的表达增强可能是其机制之一。

Objective To investigate the role of CrkL in the effect of extracellular matrix remodeling of left ventricle of post-myocardial infarction（MI）rats by β-adrenergic receptor（β-AR） over-actuation treatment.Methods MI models were established by ligating left anterior descending coronary artery.Forty SD rats were divided into MI isoprenaline groups（n=15）and MI placebo groups（n=10）,sham-operation isoprenaline groups（n=9） and sham-operation placebo groups（n=6）,which were treated with isoprenaline and physiological saline respectively.Ejection factor （EF） and fractional shortening （FS） were examined by Doppler ultrasonograph.After twelve weeks,the collagen volume fraction（CVF） was measured by Masson stained sections of cardiac muscle.The expression of CrkL protein in peri-infarction zone was detected by Western blot.Results Compared with MI placebo groups rats,isoprenaline-treated MI rats changed in several features including the aggravated heart function significantly,increased CVF sharply,and the elevated expression of CrkL protein in peri-infarction zone.Furthermore,the expression of Crkl protein herein had a positive correlation with the CVF.Conclusions β-AR over-actuation could aggravate extracellular matrix remodeling of left ventricle in post-MI rats,the elevated expression level of CrkL protein maybe one of the mechanisms.