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Magnesium taurate attenuates progression of hypertension and cardiotoxicity against cadmium chloride-induced hypertensive albino rats

机译:牛磺酸镁可减轻高血压的进展以及对氯化镉诱发的高血压白化病大鼠的心脏毒性

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摘要

The present study was designed to evaluate the antihypertensive activity and cardioprotective effects of magnesium taurate against cadmium chloride (CdCl2)-intoxicated albino rats. Sprague Dawley male albino rats (120–150 g) were divided into five groups having six animals in each group. Hypertension and cardiotoxicity were induced in animals by administration of CdCl2 (0.5 mg/kg/day, i.p.) for four weeks. Magnesium taurate (2 and 4 mg/kg/day) was administered orally after induction of hypertension (after two weeks) in their respective groups concurrently with CdCl2 for next two weeks. Amlodipine (3 mg/kg/day, p.o.) was used as a standard and administered after induction of hypertension. Blood pressure was monitored biweekly by using non-invasive blood pressure system and biochemical parameters and histopathology of the heart were evaluated after four weeks of the experimental protocol. During the four weeks of the experimental protocol, the toxic control group showed significant elevation of systolic and diastolic blood pressure concomitant with augmentation of cardiotoxicity as indicated by reduction in myocardial antioxidants including glutathione peroxidase, catalase, superoxide dismutase, reduced glutathione and increased malondialdehyde level in heart as compared to the normal group. The oral administrations of magnesium taurate significantly restored the blood pressure, myocardial antioxidants and malondialdehyde level as compared to toxic control group. In addition, histopathological examination showed that magnesium taurate treatments substantially reduced the myocardial damages against CdCl2 treatment. The results suggest that magnesium taurate has prominent antihypertensive and cardioprotective activity via its potent antioxidant activity and can be used as a nutrition supplement to improve the cardiovascular health.
机译:本研究旨在评估牛磺酸镁对氯化镉(CdCl2)中毒的白化病大鼠的抗高血压活性和心脏保护作用。将Sprague Dawley雄性白化病大鼠(120-150 g)分为五组,每组六只动物。通过施用CdCl2(0.5 mg / kg /天,腹腔注射)持续四周,可诱发动物高血压和心脏毒性。诱发高血压后(两周后)口服牛磺酸镁(2和4 mg / kg /天),接下来的两周同时口服CdCl2。氨氯地平(3 mg / kg /天,p.o.)用作标准品,在诱发高血压后给药。使用无创血压系统每两周监测一次血压,并在实验方案进行四周后评估其生化参数和心脏的组织病理学。在实验方案的四个星期中,中毒对照组显示出收缩压和舒张压的显着升高,同时伴随着心脏毒性的增加,如心肌抗氧化剂(包括谷胱甘肽过氧化物酶,过氧化氢酶,超氧化物歧化酶)减少,谷胱甘肽减少和丙二醛水平升高所表明的。心脏与正常组相比。与毒性对照组相比,口服牛磺酸镁可显着恢复血压,心肌抗氧化剂和丙二醛水平。另外,组织病理学检查表明牛磺酸镁治疗显着减少了对CdCl2治疗的心肌损害。结果表明,牛磺酸镁具有强大的抗氧化活性,具有显着的抗高血压和心脏保护作用,可作为营养补充品改善心血管健康。

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