Apocynum Tablet Protects against Cardiac Hypertrophy via Inhibiting AKT and ERK1/2 Phosphorylation after Pressure Overload.

Apocynum Tablet Protects against Cardiac Hypertrophy via Inhibiting AKT and ERK1/2 Phosphorylation after Pressure Overload.
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罗布麻片通过抑制压力过载后的 AKT 和 ERK1/2 磷酸化来预防心脏肥大

DOI:
10.1155/2014/769515
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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:
Zhang M
Zhang M
中科院分区:
其他
文献类型:
--
作者:
Qi J;Liu Q;Gong K;Yu J;Wang L;Guo L;Zhou M;Wu J;Zhang M

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背景心脏肥大发生在许多心血管疾病中。罗布麻片是一种传统中药,在我国被广泛用于治疗高血压病。然而,AT在高血压诱导的心肌肥厚中的分子机制尚不清楚。本研究旨在探讨AT对心肌肥厚的影响及其机制。方法.本研究通过横主动脉缩窄术(TAC)诱导压力超负荷建立小鼠心肌肥厚模型,并将46只小鼠分为4个研究组(AT和TAC联合),探讨AT对心肌肥厚的影响。此外,我们还利用Western blot技术对AT的心脏保护作用中ERK 1/2、AKT磷酸化的信号通路和GATA 4的蛋白表达进行了评估。结果AT可抑制术后2周ERK 1/2的Thr 202/Tyr 204位点、AKT的Ser 473位点的磷酸化和GATA 4的蛋白表达,显著抑制心肌肥厚和心肌纤维化(P < 0.05)。结论.我们的实验表明,AT抑制心肌肥厚通过抑制ERK 1/2和AKT的磷酸化。
Background. Cardiac hypertrophy occurs in many cardiovascular diseases. Apocynum tablet (AT), a traditional Chinese medicine, has been widely used in China to treat patients with hypertension. However, the underlying molecular mechanisms of AT on the hypertension-induced cardiac hypertrophy remain elusive. The current study evaluated the effect and mechanisms of AT on cardiac hypertrophy. Methods. We created a mouse model of cardiac hypertrophy by inducing pressure overload with surgery of transverse aortic constriction (TAC) and then explored the effect of AT on the development of cardiac hypertrophy using 46 mice in 4 study groups (combinations of AT and TAC). In addition, we evaluated the signaling pathway of phosphorylation of ERK1/2, AKT, and protein expression of GATA4 in the cardioprotective effects of AT using Western blot. Results. AT inhibited the phosphorylation of Thr202/Tyr204 sites of ERK1/2, Ser473 site of AKT, and protein expression of GATA4 and significantly inhibited cardiac hypertrophy and cardiac fibrosis at 2 weeks after TAC surgery (P < 0.05). Conclusions. We experimentally demonstrated that AT inhibits cardiac hypertrophy via suppressing phosphorylation of ERK1/2 and AKT.
DOI: 10.1371/journal.pone.0084591
发表时间: 2013
期刊: PloS one
影响因子: 3.7
作者:
van Berlo JH;Aronow BJ;Molkentin JD
通讯作者: Molkentin JD
DOI: 10.1161/01.cir.0000441139.02102.80
发表时间: 2014-01-21
期刊: Circulation
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通讯作者: American Heart Association Statistics Committee and Stroke Statistics Subcommittee
DOI: 10.1038/nrm3619
发表时间: 2013-08
期刊: Nature reviews. Molecular cell biology
影响因子: --
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DOI: 10.1161/01.res.0000215985.18538.c4
发表时间: 2006-03-31
影响因子: 20.1
作者:
Oka, T;Maillet, M;Molkentin, JD
通讯作者: Molkentin, JD
DOI: 10.1016/j.yjmcc.2012.10.013
发表时间: 2013-01-01
影响因子: 5
作者:
Dionyssiou, M. G.;Nowacki, N. B.;McDermott, J. C.
通讯作者: McDermott, J. C.