The protection of resveratrol and its combination with glibenclamide, but not berberine on the diabetic hearts against reperfusion-induced arrhythmias: the role of myocardial K<sub>ATP</sub> channel

Kaya, Salih Tunç; Bozdoğan, Ömer; Özarslan, Talat Oğulcan; Taşkın, Eylem; Ekşioğlu, Didem; Erim, Firdevs; Fırat, Tülin; Yaşar, Selçuk

doi:10.1080/13813455.2018.1440409

Cited by 17 publications

(11 citation statements)

References 39 publications

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“…One advantage of leptin is without to gain weight in the treatment of type 1 DM while making a balance of blood glucose. An extensive research report that type 1 DM reduces body weight [11,23] as reported in the present study. It is probably that type 1 DM causes dehydration, declining glucose utilisation and protein anabolism [10].…”

Section: Discussionsupporting

confidence: 71%

The effects of leptin on F-actin remodelling in type 1 diabetes

et al. 2019

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Background: The aim of the current study is to investigate the effect of leptin on cytoskeleton structures in both in vivo and in vitro model of diabetes. Materials and methods: For in vivo studies, leptin in different doses (240, and 480 mg/kg) was injected to the diabetic rats after 1-week of streptozotocin (STZ, 55 mg/kg) treatment. Leptin levels were analysed in serum, liver, and pancreas samples. Hepatic and pancreatic F-and G-actin expressions were determined by Western blotting. For in vitro studies, hepatic and pancreatic primary cell lines were obtained from the control rats. To these cultures, STZ (15 and 30 mM), leptin (50, 60 and 100 ng/mL), and their combinations were applied for 1, 3, and 4 weeks. After the treatment period, F-actin was visualised by the Alexa-fluor fluorescent dye. Results: Streptozotocin decreased the G-actin in both tissues in vivo. However, leptin caused a dose-dependent increase in G-actin levels while F-actin decreased in both tissues. Moreover, leptin caused the perimembranous condensation of actin filaments and amelioration of F-actin structures in vivo. A dose-dependent corruption of F-actin filament structures was observed in leptin-treated primary cells in vitro, while STZ also caused corruption of these filaments. Co-exposure of STZ and leptin caused the amelioration of F-actin filaments, while the perimembranous condensation was also observed as was in vivo study. Conclusions: Leptin therapy could be a candidate for diabetes, but it should not be ruled out as being important the severity of diabetes and leptin doses.

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Section: Discussionsupporting

confidence: 71%

The effects of leptin on F-actin remodelling in type 1 diabetes

et al. 2019

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“…Ischemia causes functional disturbance in K + homeostasis in the myocardium and plays a critical role in the genesis of ischemia/ reperfusion-induced ventricular arrhythmias (Harris et al, 1958;Tosaki et al, 1988;Curtis and Hearse, 1989). Various mechanisms of drugs by which cellular K + loss causes electrophysiological disturbances, including the function and expression of ATP-dependent K + channels, may involve the blocking and/or opening of these K + channels (Noma, 1983;Tosaki et al, 1995;Das and Sarkar, 2005;Kaya et al, 2019) at various degrees, which may aggravate or diminish the severity of ventricular arrhythmias in the ischemic/reperfused myocardium. Thus, the modification of the expression of K ATP channels by K ATP channel opener or blocker agents, respectively, can increase or decrease the incidence of ischemia/reperfusion-induced arrhythmias.…”

Section: K +mentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

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This review is focusing on the understanding of various factors and components governing and controlling the occurrence of ventricular arrhythmias including (i) the role of various ion channel-related changes in the action potential (AP), (ii) electrocardiograms (ECGs), (iii) some important arrhythmogenic mediators of reperfusion, and pharmacological approaches to their attenuation. The transmembrane potential in myocardial cells is depending on the cellular concentrations of several ions including sodium, calcium, and potassium on both sides of the cell membrane and active or inactive stages of ion channels. The movements of Na + , K + , and Ca 2+ via cell membranes produce various currents that provoke AP, determining the cardiac cycle and heart function. A specific channel has its own type of gate, and it is opening and closing under specific transmembrane voltage, ionic, or metabolic conditions. APs of sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells determine the pacemaker activity (depolarization phase 4) of the heart, leading to the surface manifestation, registration, and evaluation of ECG waves in both animal models and humans. AP and ECG changes are key factors in arrhythmogenesis, and the analysis of these changes serve for the clarification of the mechanisms of antiarrhythmic drugs. The classification of antiarrhythmic drugs may be based on their electrophysiological properties emphasizing the connection between basic electrophysiological activities and antiarrhythmic properties. The review also summarizes some important mechanisms of ventricular arrhythmias in the ischemic/ reperfused myocardium and permits an assessment of antiarrhythmic potential of drugs used for pharmacotherapy under experimental and clinical conditions.

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“…A large body of evidence supports the role of RSV in counteracting various pathways involved in cardiovascular disorders, either induced by diabetes or by other types of insults [37]; for example, RSV showed an ability to reduce oxidative stress in a myocardial ischemia -reperfusion model [38]. In addition, RSV in combination with glibenclamide protected the diabetic heart from reperfusioninduced arrhythmias [39]. After 4-weeks of STZ injection, cardiac expression of HO-1 was reduced.…”

Section: Discussionmentioning

confidence: 97%

Resveratrol protects against early cardiomyopathic changes-induced by Type-1 diabetes through a heme-oxygenase-1 dependent mechanism

Hammad

Ahmed

Heeba

et al. 2018

Journal of advanced Biomedical and Pharmaceutical Sciences

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Diabetes mellitus can be considered as a state of chronic inflammation and oxidative stress. Excessive oxidative stress is implicated in the pathogenesis of diabetic complications. Heme oxygenase-1 is an antioxidant enzyme that is upregulated in response to a variety of insults as a protective mechanism. Resveratrol (RSV) is a polyphenol that exhibits promising pharmacological effects in a variety of disease models. In this study, we investigated the role of RSV in prevention of early pathological changes in the diabetic heart as well as the role of hemeoxygenase-1 in this regard. To achieve this aim, diabetes was induced by ip injection of streptozotocin (50 mg/kg). Rats were divided into 5 experimental groups; normal control (CTR), diabetic control (DM), diabetic rats treated with RSV (DM+RSV); 10 mg/kg) in drinking water, diabetic rats treated with a combination of RSV and an HO-1 inhibitor, Zinc protoporphyrin (ZnPP), (DM + RSV+ZnPP); 10 µmole/Kg/week I.P) and diabetic rats treated with ZnPP alone (DM + ZnPP). Induction of diabetes was accompanied by a significant increase in cardiac MDA level and TGF- protein expression as well as a significant reduction in eNOS and HO-1 expression. Chronic treatment with RSV significantly attenuated the abovementioned pathological changes in addition to alleviation of diabetes-induced histopathological alterations. Furthermore, the effect of RSV was diminished when the HO-1 activity was blocked by ZnPP. In conclusion, these results demonstrate the role of HO-1 in mediating RSV protective effects against diabetes-induced early cardiomyopathy.

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The protection of resveratrol and its combination with glibenclamide, but not berberine on the diabetic hearts against reperfusion-induced arrhythmias: the role of myocardial K_ATP channel

Cited by 17 publications

References 39 publications

The effects of leptin on F-actin remodelling in type 1 diabetes

The effects of leptin on F-actin remodelling in type 1 diabetes

ArrhythmoGenoPharmacoTherapy

Resveratrol protects against early cardiomyopathic changes-induced by Type-1 diabetes through a heme-oxygenase-1 dependent mechanism

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The protection of resveratrol and its combination with glibenclamide, but not berberine on the diabetic hearts against reperfusion-induced arrhythmias: the role of myocardial KATP channel

Cited by 17 publications

References 39 publications

The effects of leptin on F-actin remodelling in type 1 diabetes

The effects of leptin on F-actin remodelling in type 1 diabetes

ArrhythmoGenoPharmacoTherapy

Resveratrol protects against early cardiomyopathic changes-induced by Type-1 diabetes through a heme-oxygenase-1 dependent mechanism

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The protection of resveratrol and its combination with glibenclamide, but not berberine on the diabetic hearts against reperfusion-induced arrhythmias: the role of myocardial K_ATP channel