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芪参胶囊在大鼠心肌梗死模型中通过MEK/ERK途径安全地增强心脏功能和血管生成。

Qishen capsule safely boosts cardiac function and angiogenesis via the MEK/ERK pathway in a rat myocardial infarction model.

作者信息

Guo Cai-Xia, Li Zhi-Yuan, Niu Jin-Bang, Fan Shuan-Cheng, Yan Si-Yu, Lu Pei-Pei, Su Yan-Ni, Ma Li-Hong

机构信息

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

Shanghai Kai Bao Pharmaceutical Co., Ltd, Shanghai, China.

出版信息

J Geriatr Cardiol. 2019 Oct;16(10):764-774. doi: 10.11909/j.issn.1671-5411.2019.10.008.

Abstract

BACKGROUND

Qishen (QS) capsules, a Traditional Chinese Medicine, has been widely used to treat coronary heart disease in China. However, evidence of its effectiveness remains unclear.

METHODS

To explore whether QS has cardioprotective efficacy and/or promotes angiogenesis after myocardial infarction (MI), we performed experiments in a preclinical rat MI model. One month after left anterior descending coronary artery ligation, the rats received either QS solution (0.4 g/kg/day) or the same volume of saline by intragastric injection for four weeks.

RESULTS

Echocardiographic and hemodynamic analyses demonstrated relatively preserved cardiac function in MI rats administered QS. Indeed, QS treatment was associated with reduced infarct scar size and heart weight index, and these beneficial effects were responsible for enhancing angiogenesis. Mechanistically, QS treatment increased phosphorylation of protein kinase B (Akt) and downregulated phosphorylation of mitogen-activated protein kinase/extracellular-regulated kinase (MEK/ERK).

CONCLUSIONS

QS therapy can improve the cardiac function of rats after MI by an underlying mechanism involving increased angiogenesis, at least partially via activation of the Akt signaling pathway and inhibition of MEK/ERK phosphorylation.

摘要

背景

芪参(QS)胶囊是一种中药,在中国已被广泛用于治疗冠心病。然而,其有效性的证据仍不明确。

方法

为探究QS在心肌梗死(MI)后是否具有心脏保护作用和/或促进血管生成,我们在临床前大鼠MI模型中进行了实验。在左冠状动脉前降支结扎1个月后,大鼠通过胃内注射接受QS溶液(0.4 g/kg/天)或相同体积的生理盐水,持续4周。

结果

超声心动图和血流动力学分析表明,给予QS的MI大鼠心脏功能相对得以保留。事实上,QS治疗与梗死瘢痕大小和心脏重量指数降低有关,这些有益作用有助于增强血管生成。机制上,QS治疗增加了蛋白激酶B(Akt)的磷酸化,并下调了丝裂原活化蛋白激酶/细胞外调节激酶(MEK/ERK)的磷酸化。

结论

QS治疗可通过增加血管生成的潜在机制改善MI后大鼠的心脏功能,至少部分是通过激活Akt信号通路和抑制MEK/ERK磷酸化实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea7b/6828606/c3cd5355e060/jgc-16-10-764-g001.jpg

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