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Am J Transl Res. 2016 May 15;8(5):2047-58. eCollection 2016.
2
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2
Qili Qiangxin capsules for chronic heart failure: A GRADE-assessed clinical evidence and preclinical mechanism.芪苈强心胶囊治疗慢性心力衰竭:一项GRADE评估的临床证据和临床前机制
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本文引用的文献

1
Modified VEGF targets the ischemic myocardium and promotes functional recovery after myocardial infarction.改良型血管内皮生长因子靶向缺血心肌,促进心肌梗死后的功能恢复。
J Control Release. 2015 Sep 10;213:27-35. doi: 10.1016/j.jconrel.2015.06.036. Epub 2015 Jul 2.
2
Qiliqiangxin inhibits angiotensin II-induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin-6.芪苈强心通过抑制白细胞介素-6抑制血管紧张素II诱导的大鼠心脏成纤维细胞转分化。
J Cell Mol Med. 2015 May;19(5):1114-21. doi: 10.1111/jcmm.12512. Epub 2015 Mar 6.
3
Traditional Chinese Medication Qiliqiangxin attenuates cardiac remodeling after acute myocardial infarction in mice.中药芪苈强心减轻小鼠急性心肌梗死后的心脏重塑。
Sci Rep. 2015 Feb 11;5:8374. doi: 10.1038/srep08374.
4
A chemical biology approach identified PI3K as a potential therapeutic target for neurofibromatosis type 2.一种化学生物学方法将 PI3K 鉴定为神经纤维瘤病 2 型的潜在治疗靶点。
Am J Transl Res. 2014 Oct 11;6(5):471-93. eCollection 2014.
5
HDAC inhibitors mitigate ischemia-induced oligodendrocyte damage: potential roles of oligodendrogenesis, VEGF, and anti-inflammation.组蛋白去乙酰化酶抑制剂减轻缺血诱导的少突胶质细胞损伤:少突胶质细胞发生、血管内皮生长因子和抗炎作用的潜在作用。
Am J Transl Res. 2014 May 15;6(3):206-23. eCollection 2014.
6
VEGF-B-induced vascular growth leads to metabolic reprogramming and ischemia resistance in the heart.血管内皮生长因子B(VEGF-B)诱导的血管生长导致心脏代谢重编程和缺血耐受性。
EMBO Mol Med. 2014 Mar;6(3):307-21. doi: 10.1002/emmm.201303147. Epub 2014 Jan 21.
7
A multicenter, randomized, double-blind, parallel-group, placebo-controlled study of the effects of qili qiangxin capsules in patients with chronic heart failure.一项关于芪苈强心胶囊治疗慢性心力衰竭患者的多中心、随机、双盲、平行分组、安慰剂对照研究。
J Am Coll Cardiol. 2013 Sep 17;62(12):1065-1072. doi: 10.1016/j.jacc.2013.05.035. Epub 2013 Jun 7.
8
Beyond anti-VEGF: dual-targeting antiangiogenic and antiproliferative therapy.超越抗 VEGF:双重靶向抗血管生成和抗增殖治疗。
Am J Transl Res. 2013 May 24;5(4):393-403. Print 2013.
9
Improvement of left ventricular remodeling after myocardial infarction with eight weeks L-thyroxine treatment in rats.左甲状腺素治疗 8 周对大鼠心肌梗死后左心室重构的改善作用。
J Transl Med. 2013 Feb 14;11:40. doi: 10.1186/1479-5876-11-40.
10
Therapeutic effects of astragaloside IV on myocardial injuries: multi-target identification and network analysis.黄芪甲苷对心肌损伤的治疗作用:多靶点鉴定和网络分析。
PLoS One. 2012;7(9):e44938. doi: 10.1371/journal.pone.0044938. Epub 2012 Sep 17.

芪苈强心胶囊对慢性心肌梗死后心力衰竭大鼠左心室重构、功能障碍及细胞凋亡的心脏保护作用。

Cardio-protecteffect of qiliqiangxin capsule on left ventricular remodeling, dysfunction and apoptosis in heart failure rats after chronic myocardial infarction.

作者信息

Liang Tuo, Zhang Yuhui, Yin Shijie, Gan Tianyi, An Tao, Zhang Rongcheng, Wang Yunhong, Huang Yan, Zhou Qiong, Zhang Jian

机构信息

State Key Laboratory of Cardiovascular Disease, Heart Failure Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 10037, China.

出版信息

Am J Transl Res. 2016 May 15;8(5):2047-58. eCollection 2016.

PMID:27347313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4891418/
Abstract

BACKGROUND

Qiliqiangxin (QL) capsule is a traditional Chinese medicine which has been approved for the treatment of chronic heart failure. Evidences proved that QL capsules further reduced the NT-proBNP levels and improved left ventricular ejection fraction in CHF patients but the evidence supporting its underlying mechanism is still unclear.

METHODS AND RESULTS

Myocardial infarction (MI) -Heart failure (HF) Sprague-Dawley ratsmodel and neonatal rat cardiac myocytes (NRCMs) were used. Animals were assigned into 4 groups, normal group (n=6), shame-operation group (n=6), MI rats 4 weeks after left anterior descending coronary artery ligation were randomized into vehicle group (n=8), QL group (n=8). QL significantly attenuated cardiac dysfunction and ventricle remodeling as echocardiography and hemodynamic measurements showed improvement in left ventricular ejection fraction, fractional shortening, ±dp/dt and left ventricular end diastolic and systolic diameters in QL treated group compared with the vehicle group. Improvements ininterstitial fibrosisand mitochondrial structures were also exhibited by Sirius Red staining, RT-PCR and electron microscopy. QL treatment improved apoptosis and VEGF expression in rats marginal infract area. Complementary experiments analyzed the improved apoptosis and up-regulate of VEGF in ischemia-hypoxia cultivated NRCMs is in an Akt dependent manner and can be reversed by Akt inhibitor.

CONCLUSION

QL capsule can improve cardiac dysfunction and ventricular remodeling in MI-HF ratsmodel, this cardiac protective efficacy may be concerned with attenuated apoptosis and cardiac fibrosis. Up-regulated VEGF expression and Akt phosphorylation may take part in this availability.

摘要

背景

芪苈强心胶囊是一种已被批准用于治疗慢性心力衰竭的中药。有证据表明,芪苈强心胶囊可进一步降低慢性心力衰竭患者的N末端B型利钠肽原(NT-proBNP)水平并提高左心室射血分数,但支持其潜在机制的证据仍不明确。

方法与结果

采用心肌梗死(MI)-心力衰竭(HF)的Sprague-Dawley大鼠模型和新生大鼠心肌细胞(NRCMs)。将动物分为4组,正常组(n = 6)、假手术组(n = 6),左冠状动脉前降支结扎4周后的MI大鼠随机分为溶剂对照组(n = 8)、芪苈强心组(n = 8)。超声心动图和血流动力学测量结果显示,与溶剂对照组相比,芪苈强心组左心室射血分数、缩短分数、±dp/dt以及左心室舒张末期和收缩末期直径均有改善,表明芪苈强心能显著减轻心脏功能障碍和心室重构。天狼星红染色、逆转录-聚合酶链反应(RT-PCR)和电子显微镜检查也显示间质纤维化和线粒体结构有所改善。芪苈强心治疗改善了大鼠梗死边缘区的细胞凋亡和血管内皮生长因子(VEGF)表达。补充实验分析了缺血缺氧培养的NRCMs中细胞凋亡的改善和VEGF的上调是以蛋白激酶B(Akt)依赖的方式进行的,并且可被Akt抑制剂逆转。

结论

芪苈强心胶囊可改善MI-HF大鼠模型的心脏功能障碍和心室重构,这种心脏保护作用可能与减轻细胞凋亡和心脏纤维化有关。VEGF表达上调和Akt磷酸化可能参与了这一作用机制。