Effects of low dose of aliskiren on isoproterenol-induced acute myocardial infarction in rats

Bin-Jaliah, Ismaeel; Hussein, Abdelaziz M.; Sakr, Hussein F.; Eid, Elsayed A.

doi:10.1556/2060.105.2018.2.11

Cited by 3 publications

(5 citation statements)

References 67 publications

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“…Apoptosis markedly shares in mediation of MI including cleaved caspase‐3, TNFα, and BAX/Bcl‐2 pathway. We found the same in ISO‐ induced MI group, and this is in line with Xu et al , Kumar et al , Jana et al , and Bin‐Jaliah et al .…”

Section: Discussionsupporting

confidence: 93%

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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: 93%

“…The ISO group received ISO (150 mg/kg/day) i.p . on the 4th and 5th day with 24 h between the two doses.…”

Section: Methodsmentioning

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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“…Group IV: Received a combination of sacubitril 30 mg/kg/day with ramipril10mg/kg/day orally for 2 weeks [11]. Group V: Received a combination of sacubitril 30 mg/kg/day with aliskiren 10 mg/kg/day orally for 2 weeks [12]. …”

Section: Methodsmentioning

confidence: 99%

“…Group V: Received a combination of sacubitril 30 mg/kg/day with aliskiren 10 mg/kg/day orally for 2 weeks [12].…”

Section: Methodsmentioning

confidence: 99%

Effects of neprilysin-renin inhibition in comparison with neprilysin-angiotensin inhibition on the neurohumoral changes in rats with heart failure

Dizaye

Ali

2019

BMC Pharmacol Toxicol

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Background The activation of neurohumoral compensatory mechanisms is a common physiological phenomenon in heart failure in order to make up for a failing heart, which will usually have a deteriorating effect on overall health condition. Many medications, such as neprilysin and angiotensin inhibitors, have recently been introduced to remediate neurohumoral changes. This study was conducted to evaluate the efficacy of the sacubitril-aliskiren combination versus the sacubitril-ramipril combination in the treatment of neurohumoral changes in rats with experimentally induced heart failure. Method Thirty Wister rats were randomly assigned into five groups each of six rats, the first group was the control group. Intraperitoneal isoprenaline injections of 5 mg/kg/day for 1 week were used to induce experimental models of heart failure in rats of the rest of experimental groups. The second group served as a positive control. Rats in the third, fourth, and fifth groups received oral daily dose of sacubitril 30 mg/kg/day, sacubitril-aliskiren 30,10 mg/kg/day, and sacubitril-ramipril 30/10 mg/kg/day respectively, for 2 weeks. Results Induction of heart failure in rats has significantly increased circulating NT-proBNP (980 ± 116.71 pg/ml), MMP9 (15.85 ± 0.57 ng/ml), troponin-I (3.09 ± 0.147 ng/ml), CK-MB (31.55 ± 1.69 ng/ml), renin (736 ± 45.8 pg/ml), urea (52.1 ± 1.57 mg/dl), and creatinine (0.92 ± 0.04 mg/dl). Significant decreases in glomerular filtration rate (7.031 ± 1.6 ml/hr./kg), urine flow (0.2761 ± 0.06 ml/h/kg), total solute excretion (0.11 ± 0.03 meq/m), and mean blood pressure (83.5 ± 2.6 mm hg) were seen in rats with heart failure. Rats treated with sacubitril combined with aliskiren or ramipril showed a statistically significant reduction of NT-proBNP, MMP9, troponin serum urea, and serum creatinine. Sacubitril-aliskiren or sacubitril-ramipril administration produced a significant increase in renin plasma level, total solute excretion, urine flow, and glomerular filtration rate. Conclusion Sacubitril in combination with aliskiren or with ramipril effectively reduced plasma cardiac biomarkers, such as CK-MB, MMP9, and NT-proBNP, in rats with heart failure. Both combinations showed significant remediation of renal function through increasing GFR, urine flow, and total solute excretion, as well as reducing plasma level of renin. Net results revealed that the sacubitril-aliskiren combination has similar remediating effects on neurohumoral changes compared to the sacubitril-ramipril combination.

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Aliskiren – A promising antioxidant agent beyond hypertension reduction

Alshahrani

2020

Chemico-Biological Interactions

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Effects of low dose of aliskiren on isoproterenol-induced acute myocardial infarction in rats

Cited by 3 publications

References 67 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

Effects of neprilysin-renin inhibition in comparison with neprilysin-angiotensin inhibition on the neurohumoral changes in rats with heart failure

Aliskiren – A promising antioxidant agent beyond hypertension reduction

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