Resveratrol protects against isoproterenol induced myocardial infarction in rats through VEGF-B/AMPK/eNOS/NO signalling pathway

Feng, Lifeng; Ren, Jun; Li, Yafei; Yang, Guowei; Kang, Licheng; Zhang, Shengzheng; Ma, Changzhen; Li, Jing; Liu, Jie; Yang, Liang; Qi, Zhi

doi:10.1080/10715762.2018.1554901

Cited by 53 publications

(27 citation statements)

References 27 publications

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“…The induction of eNOS showed protective effects against cardiac injury in different models . The inhibitory effect of ISO on eNOS is an essential contributing factor in mediation of MI with endothelial injury and vascular dysfunction . This directed our attention to investigate the role of eNOS in our model.…”

Section: Discussionsupporting

confidence: 94%

“…NO has important functions in modulating the tone of the coronary vessels, cardiomyocyte contractility, monocyte adhesion and infiltration, and smooth muscle cell proliferation . Thus, stimulation of NO release by the induction of eNOS is essential in mediating its protective effect on both heart and blood vessels . Moreover, ATP‐sensitive potassium channels (K ATP ) are widely distributed and the opening of these channels is associated with vasodilatation, antioxidant, anti‐inflammatory, and anti‐apoptotic effects with protection of blood vessels against injury and ischemia .…”

Section: Introductionmentioning

confidence: 99%

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Cardioprotective effect of hemin in isoprenaline‐induced myocardial infarction: role of ATP‐sensitive potassium channel and endothelial nitric oxide synthase

Refaie

Rifaai

Bayoumi

et al. 2020

Fundamemntal Clinical Pharma

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A B S T R A C TIschemic heart disease is a common cardiac health problem. Despite the significant advances in prevention and treatment of this disorder, its incidences and complications are very serious. So, the search for more antioxidants and anti-inflammatory agents with cardioprotective effects is an urgent task. We aimed to evaluate the effects of a heme oxygenase 1 (HO1) inducer, hemin (HEM), on isoprenaline (ISO)induced myocardial damage. Forty-five Wistar albino rats were used. Animals were treated with HEM (25 mg/kg/day) i.p. for 5 days and injected with ISO (150 mg/ kg/day) i.p. on 4th and 5th day of the experiment. Detection of the role of ATPsensitive potassium channel (K ATP ) was performed by administration of glibenclamide (GP) (5 mg/kg/day) orally 2 h before HEM. Moreover, the role of endothelial nitric oxide synthase (eNOS) was detected by coadministration of Nitro-x-L-arginine (L-NNA) (25 mg/kg/day) for 5 days. The ISO group showed increase in heart weight, cardiac enzymes, tumor necrosis factor alpha (TNFa), and malondialdehyde (MDA) with decrease in reduced glutathione (GSH), HO1, and total antioxidant capacity (TAC). In addition, there were increases in Bcl-2 associated X protein (Bax) and cleaved caspase-3, but decreases in B-cell lymphoma-2 (Bcl-2) and eNOS. Moreover, the histopathological examination of the ISO group showed degeneration of the cardiac muscle fibers and marked infiltration of the inflammatory cells. The biochemical and histopathological changes induced by ISO were markedly ameliorated in the HEM plus ISO group. This protective effect was diminished with coadministration of GP or L-NNA; thus, K ATP and eNOS might mediate HEM cardioprotection. I N T R O D U C T I O NCardiovascular diseases including myocardial infarction (MI) are among the most severe illnesses that could lead to death. MI occurs due to the imbalance between oxygen supply and oxygen demand followed by myocardial hypoxia [1]. This imbalance with the excessive release of reactive oxygen species (ROS) is a major contributing factor in the development of MI. Free radicals attack membrane lipids and mediate a chain of reactions of lipid peroxidation associated with disruption of the structure and permeability of cell membranes [2,3].Isoprenaline (ISO), a synthetic b-adrenergic agonist, causes severe oxidative stress and decreases oxygen supply in the myocardium leading to infarct-like necrosis in the heart muscles. The induction of MI using ISO is experimentally used to evaluate many cardiac ª 2019 Soci et e Franc ßaise de Pharmacologie et de Th erapeutique 302

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Cardioprotective effect of hemin in isoprenaline‐induced myocardial infarction: role of ATP‐sensitive potassium channel and endothelial nitric oxide synthase

Refaie

Rifaai

Bayoumi

et al. 2020

Fundamemntal Clinical Pharma

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“…Our results are in accordance with previous results of Shahzad et al 14 who stated that SA can scavenge ROS such superoxide and OH radicals by ameliorating the anti-oxidants such as CAT, SOD, reduced glutathioine, glutathione peroxidase and glutathione S-transferase. The results of Feng et al 29 showed that pre-treatment with RV significantly increased the activity of SOD in ISO injected rats. Moreover, Priscilla and Prince 20 have demonstrated a cardio-protection of GA against ISO-induced MI, which was mediated through both enzymatic and non-enzymatic anti-oxidants.…”

Section: Discussionmentioning

confidence: 94%

“…It has been reported that oral pre-treatment of SA significantly protected against both ISO-induced cardio-toxicity 14 and carbon tetra chloride-induced liver injury in rats 28 by reducing the marker enzymes CK-MB, LDH, alanine transaminase and aspartate transaminase in serum due to the anti-oxidant activity of SA. Additionally, Feng et al 29 showed that RV ameliorated serum cardiac marker enzymes in ISOinduced MI rats by increasing the anti-oxidant enzyme SOD. Priscilla and Prince 20 demonstrated that pre-treatment with GA in ISOinduced MI rats showed protective effect upon cardiac marker enzymes.…”

Section: Discussionmentioning

confidence: 99%

Combined cardio-protective ability of syringic acid and resveratrol against isoproterenol induced cardio-toxicity in rats via attenuating NF-kB and TNF-α pathways

Manjunatha

Shaik

Prasad

et al. 2020

Sci Rep

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the study was conducted to evaluate the cardio-protective activity of combination (coMB) of syringic acid (SA) and resveratrol (RV) against isoproterenol (iSo) induced cardio-toxicity in rats. Rats were pretreated orally with SA (50 mg/kg), RV (50 mg/kg) and combination of SA (25 mg/kg) and RV (25 mg/kg) along with positive control gallic acid (50 mg/kg) for 30 days. The effects of ISO on cardiac markers, lipid profile and lipid peroxidation marker, anti-oxidant enzymes and m-RNA expression of nuclear factorkappa B (nf-kB) and tumor necrosis factor-α (tnf-α) were observed along with histopathological observations of simple and transmission electron microscopes (teM). Serum creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and alkaline phosphatase were significantly increased while cardiac tissue CK-MB, LDH, superoxide dismutase and catalase were significantly decreased in ISO administered rats, which also exhibited a significant increase in total cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol and thiobarbutyric acid reactive substances and significant decrease in high density lipoprotein cholesterol in serum and heart. The m-RNA levels of inflammatory markers NF-kB and TNF-α were significantly increased in ISO treated rats. COMB Pre-treatment significantly reversed the ISO actions. Histopathological studies of simple and teM were also co-related with the above biochemical parameters. Docking studies with nf-kB were also performed. Evidence has shown for the first time in this approach that COMB pre-treatment ameliorated iSo induced cardio-toxicity in rats and revealed cardio-protection. A worldwide health problem, coronary artery disease (CAD), very often leads to myocardial infarction (MI). Among the patients of coronary heart disease, the principal reason for mortality worldwide is MI. As expected by World Health Organization, in 2020, most of the deaths will occur due to MI 1. According to the Global Burden of Disease 2016 Study, cardiovascular diseases (CVD) alone accounted for 24% of total burden in men and 20% of total burden in women 2. Insufficient blood supply to the myocytes leads to MI that brings about changes in electrical, mechanical, basic and biochemical properties of heart 3. Isoproterenol (ISO) is a synthetic β-adrenergic agonist used to induce acute MI 4. The main mechanism of ISOinduced myocardial ischemia is free radicals production and reactive oxygen species (ROS), oxidative stress, lipid peroxidation (LPO) and overload of calcium (Ca 2+) etc 5 .

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“…Moreover, SIRT1/AMPK attenuates palmitate-induced oxidative stress in cardiomyocytes. Multiple bioactive compounds, including curcumin (Zhang et al, 2019) and resveratrol (Feng et al, 2019) protect cardiomyocytes from apoptosis through the AMPK pathway. However, in this study, SAA did not reverse PAinduced activation of SIRT1 and AMPK phosphorylation in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of TLR4/MAPKs Pathway Contributes to the Protection of Salvianolic Acid A Against Lipotoxicity-Induced Myocardial Damage in Cardiomyocytes and Obese Mice

et al. 2021

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The occurrence of lipotoxicity during obesity-associated cardiomyopathy is detrimental to health. Salvianolic acid A (SAA), a natural polyphenol extract of Salvia miltiorrhiza Bunge (Danshen in China), is known to be cardioprotective. However, its clinical benefits against obesity-associated cardiomyocyte injuries are unclear. This study aimed at evaluating the protective effects of SAA against lipotoxicity-induced myocardial injury and its underlying mechanisms in high fat diet (HFD)-fed mice and in palmitate-treated cardiomyocyte cells (H9c2). Our analysis of aspartate aminotransferase and creatine kinase isoenzyme-MB (CM-KB) levels revealed that SAA significantly reversed HFD-induced myocardium morphological changes and improved myocardial damage. Salvianolic acid A pretreatment ameliorated palmitic acid-induced myocardial cell death and was accompanied by mitochondrial membrane potential and intracellular reactive oxygen species improvement. Analysis of the underlying mechanisms showed that SAA reversed myocardial TLR4 induction in HFD-fed mice and H9c2 cells. Palmitic acid-induced cell death was significantly reversed by CLI-95, a specific TLR4 inhibitor. TLR4 activation by LPS significantly suppressed SAA-mediated lipotoxicity protection. Additionally, SAA inhibited lipotoxicity-mediated expression of TLR4 target genes, including MyD88 and p-JNK/MAPK in HFD-fed mice and H9c2 cells. However, SAA did not exert any effect on palmitic acid-induced SIRT1 suppression and p-AMPK induction. In conclusion, our data shows that SAA protects against lipotoxicity-induced myocardial damage through a TLR4/MAPKs mediated mechanism.

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Resveratrol protects against isoproterenol induced myocardial infarction in rats through VEGF-B/AMPK/eNOS/NO signalling pathway

Cited by 53 publications

References 27 publications

Cardioprotective effect of hemin in isoprenaline‐induced myocardial infarction: role of ATP‐sensitive potassium channel and endothelial nitric oxide synthase

Cardioprotective effect of hemin in isoprenaline‐induced myocardial infarction: role of ATP‐sensitive potassium channel and endothelial nitric oxide synthase

Combined cardio-protective ability of syringic acid and resveratrol against isoproterenol induced cardio-toxicity in rats via attenuating NF-kB and TNF-α pathways

Inhibition of TLR4/MAPKs Pathway Contributes to the Protection of Salvianolic Acid A Against Lipotoxicity-Induced Myocardial Damage in Cardiomyocytes and Obese Mice

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