Time-Course of the Effects of QSYQ in Promoting Heart Function in Ameroid Constrictor-Induced Myocardial Ischemia Pigs.

Time-Course of the Effects of QSYQ in Promoting Heart Function in Ameroid Constrictor-Induced Myocardial Ischemia Pigs.
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QSYQ促进阿美罗缩蜚心肌缺血猪心功能作用的时程

DOI:
10.1155/2014/571076
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发表时间:
2014
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Wang W
Wang W
中科院分区:
其他
文献类型:
--
作者:
Qiu Q;Lin Y;Xiao C;Li C;Wang Y;Yang K;Suo W;Li Y;Chuo W;Wei Y;Wang W

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本研究旨在探讨QSYQ对猪心肌缺血(MI)模型的治疗作用及其作用机制。采用Ameroid缩窄巴马小型猪冠状动脉左前降支(LAD)建立MI模型。随机分为4组:模型组、地高辛组、芪参合剂组和假手术组。分别于术前(术后3周:0周)、给药后2、4、8周评价心功能、Ang II、cGMP、TXB 2、BNP、cTnT。给药8周后,处死猪进行心脏损伤测量。心肌梗死后,心肌组织BNP、cTnT、Ang Ⅱ、CGRP、TXB 2、ET等指标明显改变,心功能紊乱,心肌组织凋亡细胞增多。QSYQ治疗通过抵消这些事件改善心脏重塑。QSYQ的管理伴随着心脏功能和Ang II,CGRP,TXB 2,ET BNP和cTnT水平的恢复。此外,QSYQ还能减轻给药后的细胞凋亡,降低TNF-α和活性caspase-3的水平。结论:QSYQ能减轻Ameroid缩窄肌引起的心肌缺血,TNF-α和活性caspase-3可能是QSYQ的重要作用靶点。
We aim to investigate the therapeutic effects of QSYQ on a pig myocardial ischemia (MI) model and to determine its mechanism of action. The MI model was induced by Ameroid constriction of the left anterior descending coronary (LAD) in Ba-Ma miniature pigs. Four groups were created: model group, digoxin group, QSYQ group, and sham-operated group. Heart function, Ang II, CGMP, TXB2, BNP, and cTnT were evaluated before (3 weeks after operation: 0 weeks) and at 2, 4, and 8 weeks after drug administration. After 8 weeks of administration, the pigs were sacrificed for cardiac injury measurements. Pigs with MI showed obvious histological changes, including BNP, cTnT, Ang II, CGRP, TXB2, and ET, deregulated heart function, and increased levels of apoptotic cells in myocardial tissue. Treatment with QSYQ improved cardiac remodeling by counteracting those events. The administration of QSYQ was accompanied by a restoration of heart function and of the levels of Ang II, CGRP, TXB2, ET BNP, and cTnT. In addition, QSYQ attenuated administration, reduced the apoptosis, and decreased the level of TNF-α and active caspase-3. In conclusion, administration of QSYQ could attenuate Ameroid constrictor induced myocardial ischemia, and TNF-α and active caspase-3 seemed to be the critical potential target of QSYQ.
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