宣痹安痛方对心肌梗死后心室重构大鼠心功能的改善及机制

陈恒文; 李军; 林飞; 李俊平; 王阶

doi:10.13422/j.cnki.syfjx.2017230071

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宣痹安痛方对心肌梗死后心室重构大鼠心功能的改善及机制

药理 | 更新时间：2024-01-04

- 宣痹安痛方对心肌梗死后心室重构大鼠心功能的改善及机制
- Effect of Xuanbi Antong Formula in Improving Ventricular Remodeling in Myocardial Infarction Rats and Its Mechanism
- 中国实验方剂学杂志 2017年23卷第23期页码：71-78
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家科技重大专项（2013ZX09301307）;国家自然科学基金项目（81503421）
- DOI：10.13422/j.cnki.syfjx.2017230071
  中图分类号： R285.5
- 纸质出版日期：2017
- 稿件说明：
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陈恒文, 李军, 林飞, 等. 宣痹安痛方对心肌梗死后心室重构大鼠心功能的改善及机制[J]. 中国实验方剂学杂志, 2017,23(23):71-78.

CHEN Heng-wen, LI Jun, LIN Fei, et al. Effect of Xuanbi Antong Formula in Improving Ventricular Remodeling in Myocardial Infarction Rats and Its Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(23): 71-78.
陈恒文, 李军, 林飞, 等. 宣痹安痛方对心肌梗死后心室重构大鼠心功能的改善及机制[J]. 中国实验方剂学杂志, 2017,23(23):71-78. DOI： 10.13422/j.cnki.syfjx.2017230071.

CHEN Heng-wen, LI Jun, LIN Fei, et al. Effect of Xuanbi Antong Formula in Improving Ventricular Remodeling in Myocardial Infarction Rats and Its Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(23): 71-78. DOI： 10.13422/j.cnki.syfjx.2017230071.

摘要

目的：探析基于“清热活血涤痰”组方的宣痹安痛方（XBF）改善心肌梗死后心室重构大鼠心功能的作用及机制。方法：本实验采用Wistar大鼠急性心梗模型，经灌胃XBF（1.22 g·kg-1·d-1）4周后，观察XBF对大鼠体征、心脏指数的影响，超声心动图观察心功能变化，病理学检查评价心脏形态变化，酶联免疫吸附法（ELISA）评价肿瘤坏死因子-α（TNF-α），白细胞介素-6（IL-6），IL-10等细胞炎症因子的变化，免疫组化和蛋白免疫印迹法（Western blot）评价半胱氨酸蛋白酶-3（Caspase-3）和Caspase-9蛋白表达情况。结果：与模型组比较，XBF组大鼠生存状态普遍有所改善，左心室射血分数（LVEF）明显增高（P<0.05），左室舒张末内径（LVIDd）；左室收缩末内径（LVIDs）明显缩小（P<0.05）；病理学检查显示，XBF组大鼠心肌细胞变性减少，排列较整齐，肌丝较为完整，间隙较为均匀，细胞间质胶原纤维明显减少；心肌细胞线粒体超微结构清楚，膜完整，嵴致密，基质较清楚；XBF组大鼠血清中TNF-α，IL-6表达水平显著降低（P<0.01），IL-10表达水平明显升高（P<0.05）；此外，XBF组大鼠心肌组织中Caspase-3和Caspase-9蛋白表达明显下降（P<0.05）。结论：以清热活血涤痰组方的XBF能够明显改善心梗后心室重构大鼠的心功能，其改善心功能作用机制与XBF促进心室重构的炎症因子TNF-α下调，抑制IL-6，促生IL-10，抑制Caspase-3和Caspase-9的表达等因素相关。

Abstract

Objective: To evaluate the effect of Xuanbi Antong formula (XBF) on ventricular remodeling in myocardial infarction rats and its mechanism. Method: In this study

the acute myocardial infarction model was established by ligating the anterior descending coronary artery in Wistar rats. After administration with XBF (1.22 g·kg-1·d-1) for 4 weeks

the effect of XBF on apparent signs and cardiac indexes of the Wistar rats were observed

the left ventricular ejection fraction (LVEF) observed by Doppler ultrasonography

the changes in cardiac morphology were observed by pathological examination

the expressions of tumor necrosis factor-α(TNF-α)

interleukin-6 (IL-6) and IL-10 were detected by enzyme-linked immunosorbent assay (ELISA)

and the expressions of Caspase-3 and Caspase-9 were detected by immunohistochemistry and Western blot. Result: Compared with model group

the survival conditions of rats in all treatment groups were generally improved after XBF treatment

LVEF were significantly increased (P<0.05)

both LV end-diastolic inner diameter (LVIDd) and LV end-systolic inner diameter (LVIDs) were significantly reduced (P<0.05). Pathological examination showed that the myocardium degeneration of the rats treated with XBF was decreased in a good order

the myofilaments were complete

the gaps were more uniform

and the interstitial collagen fibers were significantly reduced. The mitochondrial structure of cardiomyocytes was significantly improved

the ultrastructure was clear

and the arrangement of myofilaments was more regular. TNF-α and IL-6 were decreased (P<0.01)

and IL-10 was increased (P<0.05) in rats treated with XBF. The expressions of Caspase-3 and Caspase-9 were descended in rats treated with XBF (P<0.05). Conclusion: XBF for 'clearing heat

promoting blood circulation and removing phlegm' can significantly improve the LVEF of rats after ventricular remodeling resulted in myocardial infarction. The mechanism may be that XBF can decrease and inhibit inflammatory factors for promoting ventricular remodeling

such as TNF-α and IL-6

increase inflammatory inhibitor IL-10

and inhibit the expressions of Caspase-3 and Caspase-9.

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