Abstract

The susceptibility of tissue to ischemia-reperfusion (I/R) injury is a major obstacle to tissue regeneration and cellular survival. In this study, we investigated the possible renoprotective effect of dabigatran in an experimental renal I/R model. A total of 25 rats were randomly divided into 5 equal groups. The control group was used to obtain basal values of oxidant and antioxidant biomarkers. The sham group was used to obtain renal prolidase and malondialdehyde (MDA) levels after renal ischemia (for 45 minutes) and reperfusion (for 1 hour). A standard diet was followed. Oral 15 mg/kg dabigatran etexilate was administrated to group I, intraperitoneal 250 U/kg enoxaparin sodium was administrated to group II, and intraperitoneal 250 U/kg bemiparin sodium was administrated to group III for 1 week before the renal I/R was performed. Renal tissue samples were obtained during the first hour of reperfusion to detect renal prolidase and MDA levels in these groups, after which the rats were euthanized. Renal prolidase levels were significantly higher in the sham group compared with the control group (1834.2 ± 982.3 U/g protein vs 238.8 ± 43.6U/g protein; P = .001). Lower prolidase levels were observed in groups II (838.7 ± 123.8 U/g protein) and III (1012.9 ± 302.3 U/g protein), and the lowest prolidase levels occurred in group I (533.8 ± 96.2 U/g protein; P < .05) when compared with the sham group. The MDA levels were significantly lower (P < .05) in groups I, II, and III (163.9 ± 41.5, 185.4 ± 51.0, and 138.2 ± 22.6 μmol/g protein, respectively) compared with the sham group. Dabigatran etexilate, a univalent direct thrombin inhibitor, may protect the renal tissue more effectively when compared to low-molecular-weight heparins.

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