Genistein attenuates pathological cardiac hypertrophy in vivo and in vitro

Meng, Yanyan; Zhang, Y; Ma, Zhuo; Zhou, Haoming; Ni, Jian; Liao, Hai; Tang, Qi

doi:10.1007/s00059-017-4635-5

Cited by 14 publications

(9 citation statements)

References 43 publications

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“…Genistein inhibited cardiac remodeling in pressure overload–induced cardiac hypertrophy animal models through the inhibition of the phosphorylation of p38 and PI3K–Akt signaling pathway. 56 The present study further deciphered that NXT could also inhibit the phosphorylation of p38α, and P79350 (the agonist of p38α) could partially reverse the protective effects of NXT on cardiac remodeling. Collectively, these results suggested the protective effects of NXT on suppressing cardiac remodeling partially by inhibiting the phosphorylation of p38α.…”

Section: Discussionmentioning

confidence: 83%

Naoxintong Capsule Activates the Nrf2/HO-1 Signaling Pathway and Suppresses the p38α Signaling Pathway Via Estrogen Receptors to Ameliorate Heart Remodeling in Female Mice With Postmenopausal Hypertension

Cheng

Maboh

Wang

et al. 2022

Journal of Cardiovascular Pharmacology

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:Limited treatments are available for alleviating heart remodeling in postmenopausal hypertension. The cardioprotective effect of naoxintong (NXT) has been widely accepted. This study aimed to explore the effects of NXT on pathological heart remodeling in a postmenopausal hypertension mouse model in vivo and H9c2 cardiomyocytes in vitro. In vivo, ovariectomy combined with chronic angiotensin II infusion was used to establish the postmenopausal hypertension animal model. NXT significantly ameliorated cardiac remodeling as indicated by a reduced ratio of heart weight/body weight and left ventricle weight/body weight, left ventricular wall thickness, diameter of cardiomyocytes, and collagen deposition in the heart. NXT also significantly increased the expression of estrogen receptors (ERs) and downregulated the expression of nicotinamide adenine dinucleotide phosphate oxidase 2 (Nox2). In vitro, NXT treatment greatly suppressed angiotensin II–induced cardiac hypertrophy, cardiac fibrosis, and excessive oxidative stress as proven by reducing the diameter of H9c2 cardiomyocytes, expression of hypertrophy and fibrosis markers, intracellular reactive oxygen species, and oxidative enzymes. Mechanistically, NXT significantly upregulated the expression of ERs, which activated the Nrf2/HO-1 signaling pathway and inhibited the phosphorylation of the p38α pathway. Collectively, the results indicated that NXT administration might attenuate cardiac remodeling through upregulating the expression of ERs, which activated the Nrf2/HO-1 signaling pathway, inhibited the phosphorylation of the p38α signaling pathway, and reduced oxidative stress.

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Section: Discussionmentioning

confidence: 83%

Naoxintong Capsule Activates the Nrf2/HO-1 Signaling Pathway and Suppresses the p38α Signaling Pathway Via Estrogen Receptors to Ameliorate Heart Remodeling in Female Mice With Postmenopausal Hypertension

Cheng

Maboh

Wang

et al. 2022

Journal of Cardiovascular Pharmacology

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“…[52] Further, another previous report found that genistein significantly reduced hypertrophic markers such as ANP, BNP, and β-MHC in aortic banding-induced cardiac hypertrophy. [53] Higher Ctgf expression, induced by Tgfb promoted the transformation from cardiac fibroblasts to myofibroblasts and increased ECM production. [49] Wang et al [54] reported that Tgfb (TGF-β) regulates ECM production, tissue homeostasis, and cell division.…”

Section: Discussionmentioning

confidence: 99%

Biochanin‐A alleviates fibrosis and inflammation in cardiac injury in mice

Sharma

Singh

Rana

et al. 2023

J Biochem & Molecular Tox

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Biochanin-A (BCA), is an isoflavonoid, exhibits protective effects against various diseases. This study was conducted to observe the effect of BCA on isoprenaline (ISP)-induced cardiac fibrosis and explore the underlying mechanism. The curative effect of BCA was investigated with oral administration for 14 days in ISPinduced cardiac fibrosis in mice. The fibrotic biomarkers, like collagen I and III, were estimated by ELISA. Commercial kits were used to estimate cholesterol, triglycerides, and creatine kinase-myocardial band (CK-MB) levels. The messenger ribonucleic acid (mRNA) expression studies were performed by quantitative real-time polymerase chain reaction. Gelatin zymography was used to study the expression of matrix metalloproteinases-2 (MMP-2). BCA co-administration significantly improved the morphometric parameters; including heart weight, heart weight to body weight, heart weight to tibial length, and lipid profile. BCA treatment showed a reduction in inflammatory cells and collagen deposition as depicted in the histopathology of heart tissues. The enhanced levels of collagen-I, III, and hydroxyproline were significantly decreased by BCA co-treatment, whereas CK-MB level was reduced slightly. BCA co-administration increased the activity of reduced glutathione enzyme, showing the antioxidative effects of BCA. BCA treatment significantly reduced interleukin-6 (Il6) inflammatory cytokine along with partially decreased mRNA expression of fibrotic signaling markers such as natriuretic peptide type B (Nppb), α-smooth muscle actin (Acta2), connective tissue growth factor (Ctgf), transforming growth factor β (Tgfb), small mothers against decapentaplegic homolog-3 (Smad-3). However, BCA did not modify Mmp-2 expression, which was significantly increased by ISP. In conclusion,

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“…Hence, in human aortic and porcine coronary endothelial cells, genistein enhanced eNOS expression and augmented NO synthesis (9)(10)(11). In addition, the opposite effects of genistein on iNOS/eNOS-related NO release were found to be associated with its beneficial role against isoproterenol-induced cardiac hypertrophy (12).…”

Section: Genistein Improves Viability Proliferation and Mitochondrial Function Of Cardiomyoblasts Cultured In Physiologic And Peroxidativmentioning

confidence: 92%

Genistein improves viability, proliferation and mitochondrial function of cardiomyoblasts cultured in physiologic and peroxidative conditions

et al. 2019

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Phytoestrogens exert protective effects on the cardiovascular system through mechanisms that have yet to be clearly demonstrated. The aim of this study was to evaluate the protective effects exerted by genistein on cardiomyoblasts (H9c2) against oxidative stress, nitric oxide (NO) release, viability, proliferation/migration and mitochondrial function. H9c2 cultured in physiological or peroxidative conditions, were treated with genistein in the absence or presence of estrogen receptors (ERs), G protein-coupled-estrogenic-receptors (GPER), Akt, extracellular-signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen activated protein kinase (p38MAPK) blockers. cell viability, proliferation, migration, mitochondrial membrane potential, mitochondrial oxygen consumption and oxidant/antioxidant system, were measured by specific assays. Western blot assay was used for the analysis of NO synthase (NOS) subtypes' and expression and activation of various kinases. In all experiments 17β-estradiol was used for comparison. The results showed that phytoestrogens and estrogens can increase cell viability, proliferation/migration and improve mitochondrial membrane potential and oxygen consumption of H9c2. Furthermore, NO release was modulated by genistein and 17β-estradiol. These effects were reduced or abolished by the pre-treatment with ERs, GPER, Akt, ERK1/2 and p38MAPK blockers. Finally, a reduction of reactive oxygen species production and an increase of glutathione content was found in response to the two agents. In H9c2 cultured in physiological conditions, genistein induced endothelial NOS-dependent NO production through the involvement of estrogenic receptors and by the modulation of intracellular signalling related to Akt, ERK1/2, and p38MAPK. Moreover, estrogens and phytoestrogens protected H9c2 against oxidative stress by reducing inducible NOS expression and through the modulation of the antioxidant system and mitochondrial functioning.

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Genistein attenuates pathological cardiac hypertrophy in vivo and in vitro

Abstract: Genistein attenuated pressure overload-induced cardiac hypertrophy in vivo and PE induced NRCM hypertrophy in vitro. The underlying mechanisms of genistein activity may be associated with blocking the JNK1/2 signaling pathways.

Cited by 14 publications

References 43 publications

Naoxintong Capsule Activates the Nrf2/HO-1 Signaling Pathway and Suppresses the p38α Signaling Pathway Via Estrogen Receptors to Ameliorate Heart Remodeling in Female Mice With Postmenopausal Hypertension

Naoxintong Capsule Activates the Nrf2/HO-1 Signaling Pathway and Suppresses the p38α Signaling Pathway Via Estrogen Receptors to Ameliorate Heart Remodeling in Female Mice With Postmenopausal Hypertension

Biochanin‐A alleviates fibrosis and inflammation in cardiac injury in mice

Genistein improves viability, proliferation and mitochondrial function of cardiomyoblasts cultured in physiologic and peroxidative conditions

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