Puerarin attenuates pressure overload-induced cardiac hypertrophy

Yuan, Yuan; Zong, Jing; Zhou, Haoming; Bian, Zhou‐Yan; Deng, Wei; Dai, Jia; Gan, Hua; Zheng, Yang; Li, Hongliang; Tang, Qi‐Zhu

doi:10.1016/j.jjcc.2013.06.008

Cited by 77 publications

(78 citation statements)

References 43 publications

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“…TGF-β also acts as a pro-fibrotic and proapoptotic factor in the heart. 23, 24 Thus, the suppression of TGF-β1 expression caused by GIP might contribute to the prevention of cardiac fibrosis and apoptosis, as well as cardiomyocyte enlargement. In respect to mechanisms in the suppression of TGF-β1 expression by GIP signaling, there are possibilities that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and p38 mitogen-activated protein kinase (MAPK) are involved.…”

Section: Anti-hypertrophic Effects Of Gip In Wt Micementioning

confidence: 99%

Suppressive Effects of Glucose-Dependent Insulinotropic Polypeptide on Cardiac Hypertrophy and Fibrosis in Angiotensin II-Infused Mouse Models

Hiromura

Mori

Kohashi

et al. 2016

Circ J

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Section: Anti-hypertrophic Effects Of Gip In Wt Micementioning

confidence: 99%

Suppressive Effects of Glucose-Dependent Insulinotropic Polypeptide on Cardiac Hypertrophy and Fibrosis in Angiotensin II-Infused Mouse Models

Hiromura

Mori

Kohashi

et al. 2016

Circ J

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“…However, although current pharmacological approaches appear to be beneficial in improving the quality of life of patients with heart failure, they do not markedly reduce the mortality rates (4). A previous study showed that puerarin attenuates the cardiac hypertrophy induced by pressure overload by downregulating phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) and c-Jun N-terminal kinase (JNK) signaling pathways (5). Therefore, a key future challenge is the identification of pharmacological agents that alleviate progressive myocardial dysfunction and unfavorable remodeling, improve the quality of life and reduce the mortality rate of patients with heart failure.…”

Section: Introductionmentioning

confidence: 99%

“…Naringenin is a bitter principle component of grapefruit (Citrus paradisi) that exhibits a variety of pharmacological effects, including anti-inflammatory (6), hypolipidemic, antithrombotic and antiatherogenic properties (5). The dietary consumption of citrus fruits is associated with a reduced rate of acute coronary events (7), and naringenin appears to exert beneficial effects on the cardiovascular system (8).…”

Section: Introductionmentioning

confidence: 99%

Naringenin attenuates pressure overload-induced cardiac hypertrophy

Zhang

Zheng

Yuan

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Cardiac hypertrophy is characterized by abnormal enlargement of cardiomyocytes and disproportionate accumulation of extracellular interstitial fibrosis, which are major predictors of the development of coronary artery disease and heart failure. Naringenin is a bitter principle component of grapefruit that has numerous pharmacological effects, including anti-inflammatory, hypolipidemic, antithrombotic and antiatherogenic properties. In order to investigate whether naringenin is able to exert a protective effect against cardiac hypertrophy induced by pressure overload, aortic banding (AB) was performed to induce cardiac hypertrophy in mice, and naringenin was administered for 7 weeks. A total of 60 mice were allocated into four groups: Sham + vehicle, AB + vehicle, sham + naringenin and AB + naringenin. Naringenin treatment attenuated cardiac dysfunction, as indicated by the results of echocardiography and catheter-based measurements at 8 weeks post-surgery. The extent of cardiac hypertrophy was assessed by the heart weight/body weight, heart weight/tibial length and lung weight/body weight ratios, in addition to the cardiomyocyte cross-sectional area and the mRNA expression levels of hypertrophic maker, all of which were mitigated by naringenin administration. Naringenin also inhibited the expression of transforming growth factor-β1, connective tissue growth factor, collagen Iα and collagen IIIα, and attenuated interstitial fibrosis. In addition, naringenin downregulated the activation of the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathways. In conclusion, naringenin attenuated cardiac hypertrophy and interstitial fibrosis, in addition to improving left ventricular function in pressure-overloaded mice. The cardioprotective effect exerted by naringenin may be associated with the inhibition of PI3K/Akt, ERK and JNK signaling pathways.

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“…In adult mice and rat hearts, pressure overload activates several pathways, including the mitogen-activated protein kinase pathway, resulting in hypertrophy and eventually heart failure via remodeling with fibrosis. 8,9) Mechanical stretch on isolated neonatal CMs, directly or indirectly (as in the case of paracrine secretion), induces hypertrophy via the same pathway that induces hypertrophy of adult CMs after constriction. 10) In this neonatal model, the hearts in the constriction group showed increased wall thickness without fibrosis, as well as improved hemodynamics and left ventricular ejection fraction via the CM proliferative response; however, hypertrophy was not observed.…”

Section: Article P264mentioning

confidence: 99%