Effects of Xin-Ji-Er-Kang on heart failure induced by myocardial infarction: Role of inflammation, oxidative stress and endothelial dysfunction

Hu, Juan; Cheng, Pan; Huang, Guang-yao; Cai, Guowei; Lian, Feng-zhen; Wang, Xiaoyun; Gao, Shan

doi:10.1016/j.phymed.2018.03.036

Cited by 24 publications

(18 citation statements)

References 58 publications

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“…After MI, both oxidative stress and inflammatory responses have been reported to cause myocardial injury (Nian, Lee, Khaper, & Liu, ; Hori & Nishida, ), and suppression of oxidative damage and inflammation successfully attenuates cardiac dysfunction following MI (Hu et al, ). In this study, we found that spermidine significantly inhibited oxidative stress and reduced the levels of the inflammatory cytokines following MI.…”

Section: Discussionmentioning

confidence: 99%

Spermidine‐enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway

Yan

Wang

Ling

et al. 2019

British J Pharmacology

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Background and Purpose Spermidine, a natural polyamine, is abundant in mammalian cells and is involved in cell growth, proliferation, and regeneration. Recently, oral spermidine supplements were cardioprotective in age‐related cardiac dysfunction, through enhancing autophagic flux. However, the effect of spermidine on myocardial injury and cardiac dysfunction following myocardial infarction (MI) remains unknown. Experimental Approach We determined the effects of spermidine in a model of MI, Sprague–Dawley rats with permanent ligation of the left anterior descending artery, and in cultured neonatal rat cardiomyocytes (NRCs) exposed to angiotensin II (Ang II). Cardiac function in vivo was assessed with echocardiography. In vivo and in vitro studies used histological and immunohistochemical techniques, along with western blots. Key Results Spermidine improved cardiomyocyte viability and decreased cell necrosis in NRCs treated with angiotensin II. In rats post‐MI, spermidine reduced infarct size, improved cardiac function, and attenuated myocardial hypertrophy. Spermidine also suppressed the oxidative damage and inflammatory cytokines induced by MI. Moreover, spermidine enhanced autophagic flux and decreased apoptosis both in vitro and in vivo. The protective effects of spermidine on cardiomyocyte apoptosis and cardiac dysfunction were abolished by the autophagy inhibitor chloroquine, indicating that spermidine exerted cardioprotective effects at least partly through promoting autophagic flux, by activating the AMPK/mTOR signalling pathway. Conclusions and Implications Our findings suggest that spermidine improved MI‐induced cardiac dysfunction by promoting AMPK/mTOR‐mediated autophagic flux.

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Section: Discussionmentioning

confidence: 99%

Spermidine‐enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway

Yan

Wang

Ling

et al. 2019

British J Pharmacology

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“…Samples were stained with hematoxylin for 1 min, followed by eosin staining for 10 sec at room temperature, and, then the samples were dried at room temperature and sealed. The middle part of the visual field was examined by light microscopy (magnification, ×20) and the field was assessed by three different pathologists ( 25 ).…”

Section: Methodsmentioning

confidence: 99%

miR‑127 aggravates myocardial failure by promoting the TGF‑β1/Smad3 signaling

Li²

2018

Mol Med Report

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Myocardial failure has a negative impact on the quality of human life. MicroRNA (miR) expression abnormalities lead to the development of many pathological conditions, including myocardial failure, and therefore the present study primarily focused on the investigation of the functions of miR-127 in the development of myocardial failure. The miR-127 expression levels in serum samples from patients with myocardial failure were examined. Oil red O staining was used to analyze the characteristics of the myocardium of the patients. Immunohistochemistry was used to detect fatty acid synthase (FASN), stearoyl-CoA desaturase-1 (SCD1) and mitochondrial brown fat uncoupling protein 1 (UCP1) protein expression in the myocardium of the patients. Furthermore, C57BL/6J (B6) mice were induced with 15 mg/kg of doxorubicin. Echocardiography was used to detect the histopathological alterations of the myocardial cells by comparison of the myocardial tissues from the myocardial failure animal model and normal C57BL/6 mice. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression levels of miR-127 following different induction periods and immunohistochemistry was used to detect the expression of transforming growth factor-β1 (TGF-β1) and mothers against decapentaplegic homolog 3 (Smad3). Immunofluorescence was used to detect the expression alterations TGF-β1/Smad3 when miR-127 overexpression or inhibition was established. The results of the present study indicated that myocardial failure resulted in an upregulated expression of miR-127 and severe fat accumulation. FASN, SCD1 and UCP1 were highly expressed in the myocardial failure group compared with the control. Abdominal artery contraction and the ejection fraction were significantly reduced in the DOX-induced B6 mice. The cardiomyocytes became hypertrophic, and left ventricular systolic pressure and left ventricular maximum ejection pressure were altered following DOX induction in B6 mice. The results confirmed that miR-127 regulates the expression of TGF-β1/Smad3. The potential pathological mechanism of the effect of miR-127 may be based on the upregulation of the TGF-β1/Smad3 signaling pathway.

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“…Mey., and some other ingredients as well. Numerous clinical and basic researches have revealed the protective effects of XJEK on viral myocarditis [13], MI induced cardiovascular injury [14], and 2-kidney 1-clip (2K1C) induced hypertension [15, 16]. Our previous studies have shown that the doses of XJEK from 4 to 12 g/kg/day, especially 8 g/kg/day treatment for 4 weeks, may protect against inflammation, oxidative stress, and MI induced ED in mice [17].…”

Section: Introductionmentioning

confidence: 99%

Xin-Ji-Er-Kang Alleviates Myocardial Infarction-Induced Cardiovascular Remodeling in Rats by Inhibiting Endothelial Dysfunction

Cheng

Lian

Wang

et al. 2019

BioMed Research International

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The present study was designed to elucidate the beneficial effects of XJEK on myocardial infarction (MI) in rats, especially through the amelioration of endothelial dysfunction (ED). 136 Sprague-Dawley rats were randomized into 13 groups: control group for 0wk (n = 8); sham groups for 2, 4, and 6 weeks (wk); MI groups for 2, 4, and 6 wk; MI+XJEK groups for 2, 4, and 6w k; MI+Fosinopril groups for 2, 4, and 6 wk (n = 8~10). In addition, 8 rats were treated for Evans blue staining and Tetrazolium chloride (TTC) staining to determine the infarct size. Cardiac function, ECG, and cardiac morphological changes were examined. Colorimetric analysis was employed to detect nitric oxide (NO), and enzyme-linked immunosorbent assay (ELISA) was applied to determine N-terminal probrain natriuretic peptide (NT-ProBNP), endothelin-1 (ET-1), angiotensin II (Ang II), asymmetric dimethylarginine (ADMA), tetrahydrobiopterin (BH4), and endothelial NO synthase (eNOS) content. The total eNOS and eNOS dimer/(dimer+monomer) ratios in cardiac tissues were detected by Western blot. We found that administration of XJEK markedly ameliorated cardiovascular remodeling (CR), which was manifested by decreased HW/BW ratio, CSA, and less collagen deposition after MI. XJEK administration also improved cardiac function by significant inhibition of the increased hemodynamic parameters in the early stage and by suppression of the decreased hemodynamic parameters later on. XJEK also continuously suppressed the increased NT-ProBNP content in the serum of MI rats. XJEK improved ED with stimulated eNOS activities, as well as upregulated NO levels, BH4 content, and eNOS dimer/(dimer+monomer) ratio in the cardiac tissues. XJEK downregulated ET-1, Ang II, and ADMA content obviously compared to sham group. In conclusion, XJEK may exert the protective effects on MI rats and could continuously ameliorate ED and reverse CR with the progression of MI over time.

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Effects of Xin-Ji-Er-Kang on heart failure induced by myocardial infarction: Role of inflammation, oxidative stress and endothelial dysfunction

Cited by 24 publications

References 58 publications

Spermidine‐enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway

Spermidine‐enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway

miR‑127 aggravates myocardial failure by promoting the TGF‑β1/Smad3 signaling

Xin-Ji-Er-Kang Alleviates Myocardial Infarction-Induced Cardiovascular Remodeling in Rats by Inhibiting Endothelial Dysfunction

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