Puerarin prevents cardiac hypertrophy induced by pressure overload through activation of autophagy

Liu, Bei; Wu, Zhimin; Liu, Yunpeng; Ou, Caiwen; Huang, Zhenjun; Zhang, Jianwu; Liu, Peng; Luo, Cheng; Chen, Minsheng

doi:10.1016/j.bbrc.2015.07.065

Cited by 56 publications

(42 citation statements)

References 22 publications

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“…In addition, endothelin-1, which is associated with oxidative stress and MI, has been shown to reduce myocyte autophagy [35]. β-adrenergic receptor agonist isoprenaline that increases myocardial oxidative stress [36] decreases myocyte autophagy [26]. These results are further supported by the previous report demonstrating that accumulation of ROS contributes to autophagy inhibition [37].…”

Section: Mechanisms Of Reduced Myocyte Autophagy After MIsupporting

confidence: 80%

“…The reason for the different results is unknown, but it might be related to the different species of animals or the different stages of disease. The distinct changes of myocyte autophagy have also demonstrated in pressure overload-induced cardiac hypertrophy and failure [3,5,25,26]. Role of myocyte autophagy in post-MI remodeling and dysfunction Kanamori et al have shown that the autophagy inhibitor bafilomycin A1 significantly aggravates postinfarction cardiac dysfunction and remodeling in mice [9].…”

Section: Temporal Changes Of Myocyte Autophagy After MImentioning

confidence: 99%

“…These findings are consistent with a previous report showing that myocyte autophagy was decreased during hypoxia and reoxygenization [31] in association with increased oxidative stress. Reduced myocyte autophagy also occurs in pressure overload-induced myocardial hypertrophy [3,25,26] and aging [32], all of which are associated with increased myocardial oxidative stress [33,34]. In addition, endothelin-1, which is associated with oxidative stress and MI, has been shown to reduce myocyte autophagy [35].…”

Section: Mechanisms Of Reduced Myocyte Autophagy After MImentioning

confidence: 99%

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Progressive Reduction in Myocyte Autophagy After Myocardial Infarction in Rabbits: Association with Oxidative Stress and Left Ventricular Remodeling

Chi

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: The alterations in myocyte autophagy after myocardial infarction (MI) and the underlying mechanisms have not been fully understood. In this study, we investigated the temporal changes of myocyte autophagy in the remote non-infarcted myocardium in rabbits after MI and the relationships between alterations of myocyte autophagy and left ventricular (LV) remodeling and myocardial oxidative stress. Methods: Rabbits were assigned to MI or sham operation. Rabbits with MI or sham were randomly assigned to receive chloroquine, an autophagy inhibitor, antioxidant vitamins C and E or placebo for 4 weeks. H9C2 cardiomyocytes were subjected to hypoxia or hydrogen peroxide (H 2 O 2 ) treatment. Results: MI rabbits exhibited progressive increases of LV end-diastolic dimension (EDD), and decreases of LV fractional shortening (FS) and dP/dt over 8 weeks. Myocyte autophagy assessed by the scores of LC3 and Beclin1 expression was progressively decreased at 1, 4 and 8 weeks after MI. The ratio of LC3 II/I and Beclin1 and Atg5 proteins were also decreased at 4 weeks after MI. There was a negative correlation between autophagy and LV EDD and a positive correlation between autophagy and LV FS and dP/dt. The autophagy inhibitor chloroquine worsened LV remodeling after MI. Decreased myocyte autophagy was associated with increased myocardial 4-hydroxynonenal. Antioxidant vitamins C and E prevented the decrease in myocyte autophagy after MI. In cultured H9C2 cardiomyocytes, the LC3 II/I ratio was decreased at 4 and 8 h after exposure to hypoxia, and the change was associated with increased 8-hydroxy-2-deoxyguanosine. A low concentration of H 2 O 2 decreased the LC3 II/I ratio. Conclusion: Progressive reduction in myocyte autophagy in the remote non-infarcted

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Section: Mechanisms Of Reduced Myocyte Autophagy After MIsupporting

confidence: 80%

Section: Temporal Changes Of Myocyte Autophagy After MImentioning

confidence: 99%

Section: Mechanisms Of Reduced Myocyte Autophagy After MImentioning

confidence: 99%

See 1 more Smart Citation

Progressive Reduction in Myocyte Autophagy After Myocardial Infarction in Rabbits: Association with Oxidative Stress and Left Ventricular Remodeling

Chi

Wang

et al. 2017

Cell Physiol Biochem

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“…Conversely, the activation of autophagy in response to caloric restriction, rapamycin, and metformin inhibits cardiac hypertrophy and HF . Interestingly, several studies suggest that dietary factors, including spermidine, resveratrol, and puerarin, provide cardioprotection by inducing autophagy . For example, an earlier study concluded that the oral supplementation of the natural polyamine spermidine enhances cardiac autophagy and improves cardiac hypertrophy and dysfunction, but fails to exert cardioprotective effects in the cardiomyocytes of ATG5‐deficient mice .…”

Section: Discussionmentioning

confidence: 99%

Gallic Acid Suppresses Cardiac Hypertrophic Remodeling and Heart Failure

Yan

Zhang

et al. 2018

Molecular Nutrition Food Res

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Scope Gallic acid (GA) is a dietary phenolic acid found in tea, red wine, and some plants. It exhibits anti‐oxidative and anti‐inflammatory activities. Recent studies have revealed that GA has beneficial effects against several cardiovascular diseases; however, whether GA attenuates pressure‐overload‐induced cardiac hypertrophy and the underlying mechanism remains unclear. Methods and results Primary cardiomyocyte hypertrophy is stimulated with angiotensin II (Ang II). Cardiac hypertrophic remodeling is induced in mice by transverse aortic constriction (TAC). Myocardial function is evaluated by echocardiographic and hemodynamic analyses, while cardiac tissues are analyzed by histological staining. It is observed that GA significantly decreases Ang II‐induced increases in cardiomyocyte size in vitro. Administration of GA in mice markedly improves TAC‐induced cardiac dysfunction and attenuates pathological changes, including cardiac myocyte hypertrophy, fibrosis, inflammation, and oxidative stress. Mechanistically, GA inhibits ULK1 and activates autophagy, which induces the degradation of EGFR, gp130, and calcineurin A, thereby inhibiting the downstream signaling cascades (AKT, ERK1/2, JAK2/STAT3, and NFATc1). Conclusions The results demonstrate for the first time that GA prevents myocardial hypertrophy and dysfunction via an autophagy‐dependent mechanism. Thus, GA represents a promising therapeutic candidate for treating cardiac hypertrophy and heart failure.

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“…We previously reported that treatment with PU exerts its potent ability to relieve Pb‐induced nephrotoxicity in vivo and in vitro . Meanwhile, data from other research groups indicated that PU exerts protective effects against cardiomyocyte hypertrophy or ethanol‐induced liver damage by restoring autophagy via AMPK/mTOR‐mediated signaling . Given these known activities, this paper was designed to investigate whether PU can ameliorate Pb‐induced nephrotoxicity by recovering autophagy through AMPK/mTOR signaling pathway in rPT cells.…”

Section: Introductionmentioning

confidence: 91%

Restoration of autophagy by puerarin in lead‐exposed primary rat proximal tubular cells via regulating AMPK–mTOR signaling

Song

Liu

et al. 2016

J Biochem & Molecular Tox

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Previous study has demonstrated that puerarin (PU) exerts nephroprotective effect against Pb-induced cytotoxicity in primary rat proximal tubular (rPT) cells. Autophagy can protect cells from various cytotoxic stimuli, but its role in the process of PU against Pb-induced nephrotoxicity is still unknown. This study aims to investigate whether PU can alleviate Pb-induced renal damage by recovering autophagy. Data showed that Pb inhibited the autophagic flux, as evidenced by the accumulation of LC3-II and p62 as well as the confocal microscopy analysis of GFP-LC3 puncta and punctate spots of monodansylcadaverine staining, whereas coadministration of PU could restore Pb-induced autophagy inhibition. Moreover, PU dramatically enhanced the phosphorylation of 5'AMP-activated protein kinase (AMPK) and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and its target proteins p70S6 kinase (p70S6K) and 4E-binding protein 1 (4E-BP1) in Pb-exposed rPT cells. Collectively, these evidence suggested that PU restored the impaired autophagic flux in Pb-treated rPT cells partly by activating autophagy via AMPK/mTOR-mediated signaling pathway.

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Puerarin prevents cardiac hypertrophy induced by pressure overload through activation of autophagy

Cited by 56 publications

References 22 publications

Progressive Reduction in Myocyte Autophagy After Myocardial Infarction in Rabbits: Association with Oxidative Stress and Left Ventricular Remodeling

Progressive Reduction in Myocyte Autophagy After Myocardial Infarction in Rabbits: Association with Oxidative Stress and Left Ventricular Remodeling

Gallic Acid Suppresses Cardiac Hypertrophic Remodeling and Heart Failure

Restoration of autophagy by puerarin in lead‐exposed primary rat proximal tubular cells via regulating AMPK–mTOR signaling

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