Protective effects of the standardized extract of<i>Zingiber officinale</i>on myocardium against isoproterenol-induced biochemical and histopathological alterations in rats

Amran, Athirah Z.; Jantan, Ibrahim; Dianita, Roza; Buang, Fhataheya

doi:10.3109/13880209.2015.1008147

Cited by 42 publications

(26 citation statements)

References 31 publications

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“…Various mechanism of ISO are postulated in causing myocardial infarction that includes hypoxia due to hyperactivity of myocardium and fall of pressure in coronary arteries, overload of calcium, and removal of high energy phosphate as well as production of free radicle because of auto oxidation of catecholamine leading to membrane peroxidation. The pathophysiological and morphological changes in occurring in myocardium after isoprenaline administration in rats is same with those changes which takes place in humans (Amran et al, 2015).…”

Section: Isoprenalinesupporting

confidence: 63%

A conglomeration of preclinical models related to myocardial infarction

Ahsan

Mahmood

Usmani

et al. 2020

Braz. J. Pharm. Sci.

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Cardiovascular diseases are the main source of death and morbidity in developed and developing nations. Animal models are required to propel our understanding of the pathogenesis, increase our knowledge, disease progress, and mechanism behind cardiovascular disorder, providing new approaches focused to improve the diagnostic and the treatment of these pathological conditions and additionally to test various therapeutic ways to deal with tissue regeneration and re-establish heart working following damage. A perfect model framework ought to be reasonable, effectively controlled, reproducible, and physiologically illustrative of human disease, show cardinal signs and pathology that resembles after the human ailment and ethically stable. The decision of selection of animal model should be considered precisely since it influences exploratory results and whether results of the research can be sensibly matched with the human. In this way, no specific technique splendidly reproduces the human disease, and relying upon the model, extra cost burden, resources, infrastructure and the necessity for technical hands, should also be kept under consideration. Here we have discussed and compiled various methods of inducing myocardial infarction in animals, basically by surgery, chemicals and through genetic modification, this may benefit the researchers in getting a complied data regarding various methods through which they can induce myocardial infarction in animals.

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Section: Isoprenalinesupporting

confidence: 63%

A conglomeration of preclinical models related to myocardial infarction

Ahsan

Mahmood

Usmani

et al. 2020

Braz. J. Pharm. Sci.

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“…Lower levels of HDL-c and elevated levels of LDL-c also exhibit a positive correlation with MI. Jia Ren et al 32 and Wei-Jin Fang et al 33 showed that SA and RV treatment effectively decreased the lipid profile especially LDL-c and increased the HDL-C in diabetic and cardiomyopathy rats which is due to the anti-oxidant property of SA and RV. These facts are in line with our results, where Pre-treatment with GA, SA, RV and COMB demoted the levels of TC, TG, LDL-c and VLDL-c and elevated the levels of HDL-c.…”

Section: Discussionmentioning

confidence: 99%

“…Regulation of oxidative stress was done by SOD and CAT, which are the first line of cellular defense system 33 . In ISO administered rats, decrease in the activities of anti-oxidant enzymes such as SOD and CAT were detected.…”

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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“…It is reported [44] that ethanol extract of ginger exhibited cardioprotective potential in treating myocardial injury following ISO administration. 6-Gin is a major dietary compound found in ginger.…”

Section: Discussionmentioning

confidence: 99%

[6]‐Gingerol Ameliorates ISO‐Induced Myocardial Fibrosis by Reducing Oxidative Stress, Inflammation, and Apoptosis through Inhibition of TLR4/MAPKs/NF‐κB Pathway

Han

Liu

et al. 2020

Molecular Nutrition Food Res

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Scope [6]‐Gingerol is one of the primary pungent constituents of ginger. While [6]‐gingerol has many pharmacological effects, its benefits for myocardial fibrosis, including its exact role and underlying mechanisms, remain largely unexplored. The present study is designed to characterize the cardio‐protective effects of [6]‐gingerol in myocardial fibrosis mice and possible underlying mechanisms. Methods and results Mice are subcutaneously injected with isoproterenol (ISO, 10 mg kg−1) and gavaged with [6]‐gingerol (10, 20 mg kg−1 day−1) for 14 days. Pathological alterations, fibrosis, oxidative stress, inflammation response, and apoptosis are examined. In ISO‐induced myocardial fibrosis, [6]‐gingerol treatment decreases the J‐point, heart rate, cardiac weight index, left ventricle weight index, creatine kinase (CK), and lactate dehydrogenase serum levels, calcium concentration, reactive oxygen species, malondialdehyde, and glutathione disulfide (GSSG), and increases levels of superoxide dismutase, catalase, glutathione, and GSH/GSSG. Further, [6]‐gingerol improved ISO‐induced morphological pathologies, inhibited inflammation and apoptosis, and suppressed the toll‐like receptor‐4 (TLR4)/mitogen‐activated protein kinases (MAPKs)/nuclear factor κB (NF‐κB) signaling pathways. Conclusion The protective effect of [6]‐gingerol in mice with ISO‐induced myocardial fibrosis may be related to the inhibition of oxidative stress, inflammation, and apoptosis, potentially through the TLR4/MAPKs/NF‐κB signaling pathway.

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Protective effects of the standardized extract ofZingiber officinaleon myocardium against isoproterenol-induced biochemical and histopathological alterations in rats

Cited by 42 publications

References 31 publications

A conglomeration of preclinical models related to myocardial infarction

A conglomeration of preclinical models related to myocardial infarction

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

[6]‐Gingerol Ameliorates ISO‐Induced Myocardial Fibrosis by Reducing Oxidative Stress, Inflammation, and Apoptosis through Inhibition of TLR4/MAPKs/NF‐κB Pathway

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