| Autor: |
Varkholiak I.S., Gutyj B.V., Leskiv Kh.Ya., Kushnir V.I., Hariv I.I., Martyshuk T.V., Guta, Z.A. |
| Rok vydání: |
2021 |
| Předmět: |
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| DOI: |
10.24412/2520-6990-2021-794-18-21 |
| Popis: |
The study aimed to investigate the effect of the remedy "Bendamine" on rats' antioxidant status in experimental doxorubicin-induced cardiomyopathy. The research was performed on white sexually mature young male Wistar rats weighing 180-200 g. Animals were divided into three groups of six rats each: control group intact; experimental group E1 doxorubicin was applicated intraperitoneally at a dose of 2.5 mg/kg 3 times a week for two weeks; experimental group E2 in case of doxorubicin intoxication, the drug "Bendamine" was administered intragastrically at a dose of 20 mg/kg. The action of doxorubicin and the development of the hypoxic state in rats are accompanied by activation of oxidative stress and enhancement of free radical processes. It was indicated by increased levels of intermediate and end products of lipid peroxidation and inhibition of antioxidant defense. There was a 32.7% increase in diene conjugates and a 37.6% increase in TBA-active product in rats' control groups. After application to rats, it was also found that doxorubicin causes inhibition of the glutathione system of antioxidant protection of animals. The use of the remedy "Bendamine" in the E2 group contributed to the strengthening of the enzymatic and non-enzymatic parts of the antioxidant system, protecting the structural and functional integrity of cell biomembranes. The medicine "Bendamine" inhibits the excessive formation of LPO products in pathologically altered tissues of rats' hearts. In the E2 group, the level of intermediate and final products is probably reduced. In the E2 group, the myocardial homogenate, the level of diene conjugates decreased by 16.8% also the level of TBA-active products by 20.8% compared to the E1 group-had characteristic clinical signs of cardiomyopathy caused by doxorubicin. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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