Effects of nimodipine, vinpocetine and their combination on isoproterenol-induced myocardial infarction in rats

Ansari, Mohd. Asif; Iqubal, Ashif; Ekbbal, Rustam; Haque, Syed Ehtaishamul

doi:10.1016/j.biopha.2018.10.199

Cited by 49 publications

(34 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The pathogenesis of MI is not clearly defined, but its evaluation using ISO‐induced cardiac damage demonstrated the involvement of oxidative stress, inflammation, and apoptotic pathways. Currently, ISO‐induced myocardial ischemic injury in animal models is widely used to evaluate the effects of different cardioprotective agents . For the first time, our work evaluated the possible protective effect of HEM on ISO‐induced MI and the potential roles of HO1, eNOS, and K ATP in such injury; this model is considered as a preclinical evaluation step.…”

Section: Discussionmentioning

confidence: 99%

“…ISO induces an imbalance between oxygen demand and requirement with excessive formation of free radicals leading to MI. This promotes rupture of the cardiac cell membrane with subsequent leakage of the cardiac enzymes into the bloodstream . This was also found in our study that showed significant increases of the serum levels of troponin I, LDH, and CK‐MB in the ISO group.…”

Section: Discussionmentioning

confidence: 99%

“…Free radical‐scavenging antioxidants such as GSH, glutathione peroxidase (GPx), and superoxide dismutase (SOD) are the first‐line cellular defense against oxidative stress. They eliminate oxygen radicals such as superoxide and hydrogen peroxide and prevent the formation of more reactive hydroxyl radicals . GSH is a low molecular weight thiol antioxidant.…”

Section: Discussionmentioning

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

View full text Add to dashboard Cite

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

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

show abstract

“…Nerolidol has already been reported with antioxidant, anti‐inflammatory, anticonvulsant and antimicrobial properties (Chan, Tan, Chan, Lee, & Goh, ). Recently, we have reported the protective effect of NER against cyclophosphamide‐induced cardioprotective and neuroprotective manifestations (Ansari, Iqubal, Ekbbal, & Haque, ; Iqubal, Sharma, Ansari, et al, ). Thus, NER owning antioxidant and anti‐inflammatory property can prove to be effective in counteracting gonadal toxicities induced by CP.…”

Section: Introductionmentioning

confidence: 99%

Ameliorative effect of nerolidol on cyclophosphamide‐induced gonadal toxicity in Swiss Albino mice: Biochemical‐, histological‐ and immunohistochemical‐based evidences

et al. 2020

Self Cite

View full text Add to dashboard Cite

Cyclophosphamide (CP) is commonly used as antineoplastic and immunosuppressant drug with noticeable gonadotoxic profile. Nerolidol (NER) is a sesquiterpene with potent antioxidant and anti‐inflammatory properties. Thus, the present study was designed to explore its possible gonadal protective potential against cyclophosphamide‐induced testicular, epididymal, seminal and spermatozoal toxicities. Animals were divided into five groups: control (normal saline for 14 days), treatment group (NER 200 and 400 mg/kg, p.o) for 14 days along with a single dose of cyclophosphamide (200 mg/kg, i.p) on 7th day, toxic and Per se groups (cyclophosphamide 200 mg/kg i.p) on 7th day and NER 400 mg/kg for 14 days respectively. Animals were sacrificed on the 15 day, and body weight, weight of reproductive organs, testosterone level, sperm count, biochemical parameters, histopathological and immunohistochemical studies were performed in the testes, epididymis and in the serum. CP administration induced oxidative stress, nitrative stress, inflammation, reduced testosterone level, sperm count, increased expression of MPO and caused histological aberrations in the testes, epididymis and seminal vesicles. CP caused reduced sperm count, sperm motility and testosterone level which got reversed upon treatment with nerolidol in a dose‐dependent manner. Nerolidol thus acted as a gonadoprotective molecule and prevented the gonadotoxicity of CP.

show abstract

“…Regarding the protective effect of physical activity on the heart, we aimed to estimate the potential benefits of MIT combined with nimodipine, vinpocetine, and nicardipine on systemic oxidative stress. We have chosen nimodipine, vinpocetine, and nicardipine as calcium channel modulators and PDE1 inhibitors with an antioxidant property [32].…”

Section: Discussionmentioning

confidence: 99%

Preconditioning with PDE1 Inhibitors and Moderate-Intensity Training Positively Affect Systemic Redox State of Rats

Ristić

Folić

Radonjić

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Taken into consideration that oxidative stress response after preconditioning with phosphodiesterase inhibitors (PDEIs) and moderate physical activity has still not been clarified, the aim of this study was to assess the effects of PDEIs alone or in combination with physical activity, on systemic redox status. The study was carried out on 96 male Wistar albino rats classified into two groups. The first group included animals exposed only to pharmacological preconditioning (PreC) maneuver (sedentary control (CTRL, 1 ml/day saline, n=12), nicardipine (6 mg/kg/day of NIC, n=12), vinpocetine (10 mg/kg/day of VIN, n=12), and nimodipine (NIM 10 mg/kg/day of, n=12). The second included animals exposed to preconditioning with moderate-intensity training (MIT) on treadmill for 8 weeks. After 5 weeks from the start of training, the animals were divided into four subgroups depending on the medication to be used for pharmacological PreC: moderate-intensity training (MIT+ 1 ml/day saline, n=12), nicardipine (MIT+ 6 mg/kg/day of NIC, n=12), vinpocetine (MIT+ 10 mg/kg/day of VIN, n=12), and nimodipine (MIT+ 10 mg/kg/day of NIM, n=12). After three weeks of pharmacological preconditioning, the animals were sacrificed. The following oxidative stress parameters were measured spectrophotometrically: nitrites (NO2−), superoxide anion radical (O2−), hydrogen peroxide (H2O2), index of lipid peroxidation (TBARS), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH). Our results showed that PDE1 and MIT preconditioning decreased the release of prooxidants and improved the activity of antioxidant enzymes thus preventing systemic oxidative stress.

show abstract

Effects of nimodipine, vinpocetine and their combination on isoproterenol-induced myocardial infarction in rats

Cited by 49 publications

References 45 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

Ameliorative effect of nerolidol on cyclophosphamide‐induced gonadal toxicity in Swiss Albino mice: Biochemical‐, histological‐ and immunohistochemical‐based evidences

Preconditioning with PDE1 Inhibitors and Moderate-Intensity Training Positively Affect Systemic Redox State of Rats

Contact Info

Product

Resources

About