Effect of Qishen Yiqi Dripping Pill on Oncardiac Function and Myocardial Fibrosis Associated Protein of Myocardial Infarction in Rats

ZHAO Gui-feng; WU Li-yu; XU Chuan-jia

doi:10.13422/j.cnki.syfjx.2018040131

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Effect of Qishen Yiqi Dripping Pill on Oncardiac Function and Myocardial Fibrosis Associated Protein of Myocardial Infarction in Rats

更新时间：2024-01-04

- Effect of Qishen Yiqi Dripping Pill on Oncardiac Function and Myocardial Fibrosis Associated Protein of Myocardial Infarction in Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 4, Pages: 131-136(2018)
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- DOI：10.13422/j.cnki.syfjx.2018040131
  CLC： R285.5
- Published：2018
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ZHAO Gui-feng, WU Li-yu, XU Chuan-jia. Effect of Qishen Yiqi Dripping Pill on Oncardiac Function and Myocardial Fibrosis Associated Protein of Myocardial Infarction in Rats[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(4): 131-136.
DOI：

ZHAO Gui-feng, WU Li-yu, XU Chuan-jia. Effect of Qishen Yiqi Dripping Pill on Oncardiac Function and Myocardial Fibrosis Associated Protein of Myocardial Infarction in Rats[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(4): 131-136. DOI： 10.13422/j.cnki.syfjx.2018040131.

摘要

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（Col Ⅰ），Ⅲ型胶原（Col Ⅲ），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结扎，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Col Ⅰ，Col Ⅲ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：与假手术组相比，模型组左心室内压最大上升速率（+dp/dtmax），左心室内压最大下降速率（-dp/dtmax），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Col Ⅰ，Col Ⅲ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/dtmax，-dp/dtmax，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，Col Ⅲ及PCNA，α-SMA，Vimentin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。

Abstract

Objective: To observe the effect of Qishen Yiqi dripping pill on cardiac function

collagen I (Col Ⅰ)

collagen Ⅲ(Col Ⅲ)

matrix metalloproteinase-9 (MMP-9)

proliferating cell nuclear antigen (PCNA)

α-smooth muscle actin (α-SMA) and vimentin in rats after myocardial infarction. Method: Male Wistar rats were randomly divided into five groups (n=10): sham-operation group

model group

Qishen Yiqi dripping pill (135 mg·kg-1·d-1) group (QSYQ-N)

Qishen Yiqi dripping pill (270 mg·kg-1·d-1) group (QSYQ-H) and captopril group. The sham-operation group was not ligated after threading. The left anterior descending coronary artery was ligated to establish the myocardial infarction model in the remaining groups. The model was evaluated by electrocardiograph(ECG). Rats were fed for 4 weeks. After 4 weeks

the hemodynamic state of rats was recorded by physiological recorder. The immunohistological method was used to detect myocardial Col Ⅰ

Col Ⅲ and PCNA

α-SMA

Vimentin expression in rats

and the enzyme linked immunosorbent assay (ELISA) was used to detect MMP-9 concentration in rat serum. Result: Compared with the sham-operation group

+dp/dtmax

-dp/dtmax and LVSP in the model group were significantly lower

while LVEDP was significantly elevated (P<0.01). Expressions of myocardial Col Ⅰ

Col Ⅲ and PCNA

α-SMA

Vimentin in the model group were increased

and serum MMP-9 concentration was increased (P<0.01). Compared with the model group

+dp/dtmax

-dp/dtmax

LVSP in QSYQ-N

QSYQ-H and captopril groups were elevated (P<0.05

P<0.01)

while LVEDP in QSYQ-H and captopril groups was lower (P<0.05

P<0.01). Expressions of myocardial Col Ⅰ

Col Ⅲ and PCNA

α-SMA

Vimentin in QSYQ-N

QSYQ-H and captopril groups were down-regulated

and serum MMP-9 concentration decreased (P<0.05

P<0.01). Conclusion: Qishen Yiqi dripping pill can improve cardiac systolic and diastolic function in rats after myocardial infarction

and its mechanism might be correlated with the inhibition of deposition of collagen

the degradation of matrix metalloproteinase and the proliferation and differentiation of fibroblasts and myofibroblasts.

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