期刊
SURGICAL NEUROLOGY
卷 72, 期 2, 页码 146-152出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.surneu.2008.07.004
关键词
Atorvastatin; Brain edema; Traumatic brain injury; Lipid peroxidation
Background: The neuroprotective effects of statins possibly depend on their pleiotropic effect such as antioxidative and anti-inflammatory properties. In this study, we have evaluated the efficiency of atorvastatin on brain edema, lipid peroxidation, and ultrastructural changes in TBI animal model. Methods: Modified Feeney method has been used for the trauma model in rats. Only craniectomy for group A and trauma after craniectomy for group B was the procedure for animals. For the trauma, rods weighing 24 g were dropped on a foot plate just over the dura. Atorvastatin (1 mg/kg, IP) was administered to the animals in group C after craniectomy and trauma; but on the other hand, animals in group D received only 0.5 mL PEG as the vehicle. Brains were harvested 24 hours after the trauma for the assays of wet-dry weight, lipid peroxidation level, and ultrastructural investigations. Lipid peroxidation levels, TEM, and UNGS were the investigated parameters. The statistical comparisons between the groups were investigated by 1-way ANOVA and post hoc analysis by Duncan and Dunnett T3 test within the groups at the significance level P = .05. Results: Trauma increased water contents of the brain tissues and lipid peroxidation levels in groups B and D. When compared with the results of group B (brain edema, 84.694% +/- 1.510%; lipid peroxidation, 74.932 +/- 2.491 nmol/g tissue), atorvastatin (1 mg/kg) significantly decreased brain edema (77.362% +/- 1.448%), lipid peroxidation level (58.335 +/- 3.980 nmol/g tissue), and UNGS scores in group C (P < 0.05). Conclusion: In this descriptive study, the remarkable improvements of atorvastatin on brain edema, lipid peroxidation, and ultrastructural investigations encouraged us for a further dose optimization study. (C) 2009 Elsevier Inc. All rights reserved.
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