Puerarin inhibits angiotensin II-induced cardiac hypertrophy via the redox-sensitive ERK1/2, p38 and NF-κB pathways

Chen, Gang; Pan, Shiqi; Shen, Cong; Pan, Shi-fen; Zhang, Xiumin; He, Qing

doi:10.1038/aps.2013.185

Cited by 50 publications

(39 citation statements)

References 35 publications

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“…Accumulated data show that CMs are remodeled or "dedifferentiated" in pathological conditions, i.e. heart failure and other cardiovascular diseases, presenting enhanced proliferation ability and morphological and functional properties similar to embryonic CMs [10,11]. Based on the myocardial protection effects of puerarin reported previously, we hypothesized that puerarin might also inhibit CM proliferation, thus further support its potential effect on reversing cardiac phenotypic remodeling in heart diseases.…”

Section: Introductionmentioning

confidence: 62%

Puerarin Exerts a Delayed Inhibitory Effect on the Proliferation of Cardiomyocytes Derived from Murine ES Cells via Slowing Progression through G2/M Phase

Luo

Zhong

Hong

et al. 2016

Cell Physiol Biochem

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Objective: Puerarin, which shows beneficial and protective effects on cardiovascular diseases, is the main isoflavone extracted from Pueraria lobata (kudzu) root. The aim of this study was to investigate the effects of puerarin on in vitro myocardial proliferation and its underlying mechanism. Methods: Myocardial differentiation of transgenic embryonic stem (ES) cells was performed by embryoid body-based differentiation method. The proliferation assay of cardiomyocytes (CMs) derived from ES cells (ES-CMs) was performed by EdU (5-Ethynyl-2'-deoxyuridine) staining. Flow cytometry was employed to determine the cell cycle distribution and apoptosis of purified ES-CMs. Quantitative real-time PCR was utilized to study the transcription of genes related to cell cycle progression. Signaling pathways relating to proliferation were studied by western blot analysis and application of specific inhibitors. Results: Puerarin exerted a delayed inhibitory effect on the proliferation of ES-CMs at the early-stage differentiation. Meanwhile, puerarin slowed progression through G2/M phase without inducing apoptosis of ES-CMs. Further assays showed that puerarin up-regulated the transcription of Cyclin A2, Cyclin B1 and Cdk1 in ES-CMs. The ERK1/2 specific inhibitor PD0325901 and the PI3K specific inhibitor Wortmannin successfully reversed puerarin-induced up-regulation of Cdk1 but not Cyclin A2 and B1. Conclusion: These findings suggest that puerarin inhibits CM proliferation via slowing progression through G2/M phase during early-stage differentiation.

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Section: Introductionmentioning

confidence: 62%

Puerarin Exerts a Delayed Inhibitory Effect on the Proliferation of Cardiomyocytes Derived from Murine ES Cells via Slowing Progression through G2/M Phase

Luo

Zhong

Hong

et al. 2016

Cell Physiol Biochem

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“…Moreover, previous reports have established a significant role of the ERK pathway to hypertrophic gene expression induced by hypertrophic agonists using an MEK-1 specific inhibitor and cDNA gene expression profiling in cardiac myocytes [64,65]. In another study it was reported that Ang II-induced CH by activation of the redox-sensitive ERK1/2, p38, and the NF-κB pathways in C57BL/6J mice which is attenuated by Pue, an isoflavone polyphenolic antioxidant [66].…”

Section: Discussionmentioning

confidence: 96%

Buthionine sulfoximine, an inhibitor of glutathione biosynthesis, induces expression of soluble epoxide hydrolase and markers of cellular hypertrophy in a rat cardiomyoblast cell line: Roles of the NF-κB and MAPK signaling pathways

Abdelhamid

El‐Kadi

2015

Free Radical Biology and Medicine

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“…This G␣ 13 -initiated cascade is independent of ANG II-activated G␣ q/11 signaling that was earlier linked to pathological cardiac hypertrophy (1143). RhoA is also a downstream effector of Nox-induced ROS in response to ANG II treatment (49,746), as are various redox-sensitive kinases and transcription factors linked to cardiac hypertrophy (148,567,1107).…”

Section: Ang II In Cardiac Hypertrophymentioning

confidence: 94%

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

Forrester

Booz

Sigmund

et al. 2018

Physiological Reviews

783

780

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The renin-angiotensin-aldosterone system plays crucial roles in cardiovascular physiology and pathophysiology. However, many of the signaling mechanisms have been unclear. The angiotensin II (ANG II) type 1 receptor (ATR) is believed to mediate most functions of ANG II in the system. ATR utilizes various signal transduction cascades causing hypertension, cardiovascular remodeling, and end organ damage. Moreover, functional cross-talk between ATR signaling pathways and other signaling pathways have been recognized. Accumulating evidence reveals the complexity of ANG II signal transduction in pathophysiology of the vasculature, heart, kidney, and brain, as well as several pathophysiological features, including inflammation, metabolic dysfunction, and aging. In this review, we provide a comprehensive update of the ANG II receptor signaling events and their functional significances for potential translation into therapeutic strategies. ATR remains central to the system in mediating physiological and pathophysiological functions of ANG II, and participation of specific signaling pathways becomes much clearer. There are still certain limitations and many controversies, and several noteworthy new concepts require further support. However, it is expected that rigorous translational research of the ANG II signaling pathways including those in large animals and humans will contribute to establishing effective new therapies against various diseases.

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Puerarin inhibits angiotensin II-induced cardiac hypertrophy via the redox-sensitive ERK1/2, p38 and NF-κB pathways

Abstract: Pue attenuates Ang II-induced cardiac hypertrophy by inhibiting activation of the redox-sensitive ERK1/2, p38 and the NF-κB pathways.

Cited by 50 publications

References 35 publications

Puerarin Exerts a Delayed Inhibitory Effect on the Proliferation of Cardiomyocytes Derived from Murine ES Cells via Slowing Progression through G2/M Phase

Puerarin Exerts a Delayed Inhibitory Effect on the Proliferation of Cardiomyocytes Derived from Murine ES Cells via Slowing Progression through G2/M Phase

Buthionine sulfoximine, an inhibitor of glutathione biosynthesis, induces expression of soluble epoxide hydrolase and markers of cellular hypertrophy in a rat cardiomyoblast cell line: Roles of the NF-κB and MAPK signaling pathways

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

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