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目的:观察芪参益气滴丸对心肌梗死后大鼠心功能,Ⅰ型胶原(colⅠ),Ⅲ型胶原(colⅢ),基质金属蛋白酶-9(MMP-9)及增殖细胞核抗原(PCNA),α-平滑肌肌动蛋白(α-SMA),波形蛋白(Vimentin)表达的影响。方法:雄性Wistar大鼠50只随机分为5组:假手术组,模型组,芪参益气滴丸低、高(135,270 mg·kg~(-1)·d~(-1))剂量组(QSYQ-N,QSYQ-H),卡托普利组,每组10只。假手术组开胸穿线不接扎,其余各组结扎左冠状动脉前降支制作心肌梗死模型,灌胃4周。4周后生理记录仪记录血流动力学状态,免疫组织化学法检测大鼠心肌ColⅠ,ColⅢ及PCNA,α-SMA,Vimentin表达,酶联免疫吸附法(ELISA)检测大鼠血清中MMP-9浓度。结果:与假手术组组相比,模型组左心室内压最大上升速率(+dP/df_(max)),左心室内压最大下降速率(-dp/dt_(max)),左心室收缩压(LVSP))均明显降低,左心室舒张末期压(LVEDP)明显升高(P<0.01);心肌ColⅠ,ColⅢ及PCNA,α-SMA,Vimentin表达上调,血清MMP-9浓度升高(P<0.01);与模型组相比,QSYQ-N,QSYQ-H组,卡托普利组+dp/dr_(max),-dP/dt_(max),LVSP提高(P<0.05,P<0.01);QSYQ-H组、卡托普利组LVEDP降低(P<0.05,P<0.01);QSYQ-N,QSYQ-H及卡托普利组大鼠心肌Col I,ColⅢ及PCNA,α-SMA,Vimenthi表达下调,MMP-9浓度降低(P<0.05,P<0.01)。结论:芪参益气滴丸能够改善心肌梗死后大鼠心脏收缩与舒张功能,其机制与抑制胶原沉积、基质蛋白的降解及心脏成纤维细胞、肌成纤维细胞增殖、分化有关。
Objective: To observe the effects of Qishen Yiqi drop pill on cardiac function, col Ⅰ, col Ⅲ, MMP-9 and PCNA in myocardial infarction rats, α-smooth muscle actin (α-SMA), vimentin (Vimentin) expression. Methods: Fifty male Wistar rats were randomly divided into 5 groups: sham operation group, model group, Qishen Yiqi dripping pill low dose group (135,270 mg · kg -1 · d -1) (QSYQ-N, QSYQ-H), captopril group, 10 in each group. Thoracotomy was performed on the sham-operated group and the left anterior descending coronary artery was ligated for the other 4 weeks. Four weeks later, the hemodynamic status was recorded by physiology recorder. The expression of ColⅠ, Col Ⅲ and PCNA, α-SMA and Vimentin in myocardium of rats were detected by immunohistochemical method. The levels of MMP-9 in serum were detected by enzyme linked immunosorbent assay (ELISA) concentration. Results: Compared with sham operation group, the maximal rate of increase of left ventricular pressure (+ dP / df max), -dp / dt max (-dp / dt max), left ventricular systolic pressure (P <0.01). The expression of ColⅠ, Col Ⅲ and PCNA, α-SMA and Vimentin in myocardium were up-regulated and the level of serum MMP-9 was increased (P < 0.01). Compared with model group, the dp / dr max, dp / dt max and LVSP in QSYQ-N, QSYQ-H group and captopril group were significantly higher than those in model group (P0.05, P0.01) ; QSYQ-H group and captopril group LVEDP decreased (P <0.05, P <0.01); QSYQ-N, QSYQ-H and captopril group myocardial Col I, Col Ⅲ and PCNA, α-SMA, The expression of Vimenthi was down-regulated and the concentration of MMP-9 was decreased (P <0.05, P <0.01). Conclusion: Qishenyiqi Dripping Pill can improve cardiac systolic and diastolic function in rats after myocardial infarction. Its mechanism is related to the inhibition of collagen deposition, the degradation of matrix protein and the proliferation and differentiation of cardiac fibroblasts and myofibroblasts.