Ginsenoside Re Attenuates Isoproterenol‐Induced Myocardial Injury in Rats

Wang, Quan-wei; Yu, Xiaofeng; Xu, Huali; Jiang, Yichuan; Zhao, Xin

doi:10.1155/2018/8637134

Cited by 18 publications

(18 citation statements)

References 24 publications

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“…ISO‐induced oxidative stress was assessed in our study that showed a marked increase in MDA, but a depletion of cardiac tissue GSH and serum TAC levels indicating the occurrence of severe lipid peroxidation and oxidative stress. These results are in line with Tkachenko et al , Wang et al , and Shahzada et al .…”

Section: Discussionsupporting

confidence: 92%

“…Troponin, CK‐MB, and LDH of cardiomyocytes leak out of the damaged tissues to the blood stream after myocardial injury. Therefore, the elevation of the serum levels of these cardiac biomarkers is an important indicator of the early detection of myocardial tissue damage .…”

Section: Discussionsupporting

confidence: 87%

“…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 .…”

Section: Introductionmentioning

confidence: 99%

“…Reduced glutathione (GSH) is a carrier of an active thiol group in the form of a cysteine residue. It acts as an antioxidant by interacting with ROS and serving as a cofactor for various antioxidant enzymes .…”

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: 92%

Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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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“…The color developed was read at 412 nm. Protein in the tissue homogenate was determined by the method of Lowry et al, (1951) 24 . The CO-NH group (peptide bond) present in the protein molecule reacts with copper sulfate in an alkaline medium to give a blue color, which was read at 620 nm.…”

Section: Estimation Of Enzymatic and Non-enzymaticmentioning

confidence: 99%

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2020

IJPSR

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The present study was designed to investigate the cardioprotective effect of Arbutin (ARB) against isoproterenol (ISO) induced myocardial infarction (MI) in rats by studying cardiac and hepatic markers, antioxidant defense system, lipid peroxidation products and histopathological changes. Rats were pretreated with ARB (25 and 50 mg/kg BW) for 21 days. After pretreatment, ISO (60 mg/kg BW) was administered subcutaneously into the rats at an interval of 24 h for 2consecutive days to induce MI. In the present study ISO-induced myocardial damage was indicated by the increased heart weight to body weight ratio and the increased activity of marker enzymes such as CK, CK-MB, ALT, AST, LDH, and the elevated levels of troponin T and I in the serum. In addition, the levels of lipid peroxidation products such as TBARS, CDs, and LHPs were significantly increased in the plasma and heart tissue of ISO rats. Activities of enzymic antioxidants such as SOD, CAT, GPx, GST and the non-enzymic antioxidants like vitamin C, vitamin E and reduced glutathione (GSH) were decreased in the erythrocytes, plasma and heart tissues of the ISOadministered rats. Histopathological observations substantiate with the biochemical parameters. The 50 mg/kg BW of ARB was more pronounced than the 25 mg/kg BW and brought back all the above parameters to near normal. ARB ameliorates myocardial damage caused by ISO in rats and provides cardioprotective effect by scavenging the free radicals, restoring the endogenous antioxidants, preserving histopathology of the myocardium and by improving the cardiac function.

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A review on herbal Nrf2 activators with preclinical evidence in cardiovascular diseases

Syed

Ram

Murty

et al. 2021

Phytotherapy Research

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Cardiovascular diseases (CVDs) are an ever‐growing problem and are the most common cause of death worldwide. The uncontrolled production of reactive oxygen species (ROS) and the activation of ROS associated with various cell signaling pathways with oxidative cellular damage are the most common pathological conditions connected with CVDs including endothelial dysfunction, hypercontractility of vascular smooth muscle, cardiac hypertrophy and heart failure. The nuclear factor E2‐related factor 2 (Nrf2) is a basic leucine zipper redox transcription factor, together with its negative regulator, kelch‐like ECH‐associated protein 1 (Keap1), which serves as a key regulator of cellular defense mechanisms to combat oxidative stress and associated diseases. Multiple lines of evidence described here support the cardiac protective property of Nrf2 in various experimental models of cardiac related disease conditions. In this review, we emphasized the molecular mechanisms of Nrf2 and described the detailed outline of current findings on the therapeutic possibilities of the Nrf2 activators specifically from herbal origin in various CVDs. Based on evidence from various preclinical experimental models, we have highlighted the activation of Nrf2 pathway as a budding therapeutic option for the prevention and treatment of CVDs, which needs further investigation and validation in the clinical settings.

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Ginsenoside Re Attenuates Isoproterenol‐Induced Myocardial Injury in Rats

Cited by 18 publications

References 24 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

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A review on herbal Nrf2 activators with preclinical evidence in cardiovascular diseases

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