engleski

Effects of enoxaparine on oxidative lipid damage and activities of antioxidant enzymes in parietal cortex and hippocampus following traumatic brain injury in rats

Enoxaparin, a low-molecular weight heparin diminishes the brain edema, and improves the functional outcomes following experimental traumatic brain injury (TBI). Molecular and cellular mechanisms involved in mentioned drug effects are not known. Present study was designed with the aim to examine whether enoxaparin affects oxidative lipid damage and antioxidant enzymes’ activities in the parietal cortex and hippocampus 48 h after the TBI induction in the rat. Experiments were carried out on adult male rats. TBI of moderate severity was performed over the left parietal cortex using the lateral fluid percussion brain injury model. Enoxaparin (1 mg/kg) or vehicle were administered i.p. 1h after TBI followed by additional 7 injections administered in intervals of 6 h. Rats were sacrificed 48 h after the TBI induction. Levels of the brain lipid peroxidation were determined by thiobarbituric acid reactive substances (TBARS) assay. Activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined by spectrophotometric measurements. Results: Cortical and hippocampal TBARS levels in rats with TBI were higher in relation to the values registered in sham-operated animals. In the left parietal cortex of enoxaparin-treated rats with TBI, SOD and GSH-Px activities were higher in comparison to injured, vehicle treated rats. In the left hippocampus of rats with TBI, enoxaparin decreased the TBARS level and increased the GSH-Px activity. Our results for the first time suggest that in TBI enoxaparin may protect the brain structures by diminishing oxidative lipid damage and increasing antioxidant enzymes’ activities.

traumatic brain injury; enoxaparin; oxidative stress; antioxidant enzymes; rats

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