5 research outputs found

    Evaluation of cardioprotective effects of the incritinmimetics exenatideand vildagliptin in the experiment

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    The results of experimental and clinical trials make it clear that incretin mimetics possess pleiotropic effects and demonstrate the value in terms of assessment of their potential opportunities as cardioprotectors. Goals: To study the cardioprotective effects of exenatide and vildagliptin on the model of doxorubicin-induced cardiomyopath

    Possible ways of pharmacological correction of ischemic damage to the liver with the agonist of peripheral imidazoline receptors C7070

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    We glad to introduce several variants of pharmacological correction of ischemic hepatic injury by imidazoline I2 receptor agonist С7070. Materials and methods: The experiment was carried out on 70 rats of both sexes, divided into 7 groups (n = 10). The indicated agonists of peripheral imidazoline I2receptors (C7070) significantly reducesischemically-reperfusion injury of the liver, in comparison with the preparations of moxonidine and metformine. Indirect sign of imidazoline activating mechanism of C7070 is decreasing of the hepatoprotective effect of C7070 by the preliminary administration of imidazoline receptor blocker BU-22

    Possible ways of pharmacological correction of ischemic damage to the liver with the agonist of peripheral imidazoline receptors C7070

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    We glad to introduce several variants of pharmacological correction of ischemic hepatic injury by imidazoline I2 receptor agonist С7070. Materials and methods: The experiment was carried out on 70 rats of both sexes, divided into 7 groups (n = 10). The indicated agonists of peripheral imidazoline I2receptors (C7070) significantly reducesischemically-reperfusion injury of the liver, in comparison with the preparations of moxonidine and metformine. Indirect sign of imidazoline activating mechanism of C7070 is decreasing of the hepatoprotective effect of C7070 by the preliminary administration of imidazoline receptor blocker BU-22

    Evaluation of cardioprotective effects of the incritinmimetics exenatideand vildagliptin in the experiment

    No full text
    The results of experimental and clinical trials make it clear that incretin mimetics possess pleiotropic effects and demonstrate the value in terms of assessment of their potential opportunities as cardioprotectors. Goals: To study the cardioprotective effects of exenatide and vildagliptin on the model of doxorubicin-induced cardiomyopath

    CARDIOPRODUCTIVE EFFECTS OF EXXENATE AMID AND VILDAGLIPTIN INCRETIN MIMETICS IN DOXYRUBRICINE CARDIOMYOPATHY MODELING

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    Aim. To study the cardioprotective effects of exenatide and vildagliptin on the doxorubicin model of cardiomyopathy.Material and methods. In the experiments at the isolated the Langendorff heart of the rat, the cardioprotective effect of exenatide (10 μg/kg/day) (Baeta®, Eli Lilly and Company, USA) and vildagliptin (0.2 mg/kg/day) (Galvus®, Novartis, Switzerland), on the contractile function of an isolated heart that underwent anterior doxorubicin (20 mg/kg, intraperitoneally for 48 hours) pathology was evaluated. Cardioprotective effect was assessed by the results of a functional test with highfrequency stimulation (480 bpm) under conditions of hypercalcium (5 mmol) perfusion.Results. The results show that the exenatide (10 μg/kg/day) and vildagliptin (0.2 mg/kg/day) incretin mimetics show a cardioprotective effect on the doxyrubicin pathology model, which is expressed in a decrease in the coefficient of diastolic dysfunction (StTTI), respectively, to 5.3±0.1 cu and 6.5±0.2 cu compared with the control group 8.3±0.1 cu.Conclusion. An assumption is made about the way of realization of the cardioprotective effect of incretin mimetics by increasing the expression of gem-oxygenase-1 (HO-1). This prevents the heme-catalyzed formation of highly active hydroxyl radicals from hydrogen peroxide. Induction of heme oxygenase-1 is accompanied by an increase in ferritin activity, which has an antiapoptotic effect due to the fact that ferritin binds excess free iron in cells subjected to oxidative stress
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