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Year : 2019  |  Volume : 5  |  Issue : 1  |  Page : 8-14

Nebivolol prevents the increase of asymmetric dimethylarginine and oxidants in hyperhomocysteinemic rats

Department of Cardiology, Faculty of Medicine, Bezmialem Vakif University, Istanbul, Turkey

Correspondence Address:
Dr. Mustafa Ahmet Huyut
Department of Cardiology, Faculty of Medicine, Gaziosmanpasa Hospital, Yeni Yuzyil University, Cukurcesme Caddesi No: 51 Istanbul
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJCA.IJCA_37_18

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Objective: The objective of this study was to determine nebivolol's inhibitory effect on endothelial dysfunction in hyperhomocysteinemic rats, based on heart pathology and biochemical analysis of serum samples. Methods: Male Wistar albino rats weighing between 200 g and 450 g were randomly divided into four groups of equal number (n = 7) as follows: control group, nebivolol group, methionine group, and methionine + nebivolol group. After 28 days, homocysteinemia (Hcy), asymmetric dimethylarginine (ADMA), malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT) levels were measured in blood samples and compared between groups. Each rat's hearts were dissected to observe cardiomyocyte degeneration; findings were compared between groups. Results: Moderate hyperHcy (hHcy) (Hcy 35.62 ± 7.60 μmol/L) was noted in methionine group (P < 0.001). The levels of the antioxidant molecules CAT, GSH, GPx, GR, and SOD were lower, and the levels of the oxidant molecules ADMA, Hcy, and MDA were higher in methionine group (P < 0.001). A decrease in antioxidants and also increase in oxidants did not occur in the methionine + nebivolol group (P < 0.001). Cardiomyocyte degeneration was more severe in methionine group (P = 0.01). Conclusion: Endothelial dysfunction induced through short-term hHcy can be prevented through the administration of nebivolol. Nebivolol can prevent elevation of the Hcy levels, and hHcy might cause cardiomyocyte degeneration.

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