Endocrine Abstracts

Objectives-Aim: Oxidized low-density lipoprotein (LDL) seems to play an important role in the etiology of atherosclerosis. They stumulate atherosclerosis. Glucocorticoids decrease LDL degradation and expression of LDL receptor. Morever insulin resistance in glucocorticoid excess state may contribute to LDL oxidation changes. The aim of this study was to investigate, the LDL oxidation in glucocorticoid excess state and the effect of atorvastatin on LDL oxidation.

Materials- Methods: Twenty four Sprague-Dawley rats were assigned to study in three groups. (1) Normal rats (2) Glucocorticoid treatment group (GT) They were given methylprednisolone 15 mg/kg/day for 8 weeks. (3) Atorvastatin treatment group (AT). These group's rats at first were given metilprednisolone 15/mg/kg/day S. C. for 8 weeks. After then, they were given 5 mg/kg/day atorvastatin by gavaj for 6 weeks. All rats were sacrificed at the end of the study. The oxidizability of LDL by determining the levels of Malonaldehyde bis(dimethyacetyl) (MDA) were determined at baseline LDL oxidation was assessed by measure of d MDA values. The MDA values were compared among normal, GT and AT groups. Mann Whitney U test was used for statistical analysis (SPSS 8,0 for Windows) and p <0.05 values were accepted as significantly.

Results: LDL oxidation was increased by glucocorticoid therapy. While MDA value was 0.253 ± 0.03 nmol/gr in the normal rats, MDA was 0.514 ± 0.29 nmol/gr in the GT group. (p=0.007). After atorvastatin therapy, LDL oxidation decreased significantly. The MDA values of the AT group was found significantly lesser than MDA values of the GT groups. (0.276 ± 0.14 nmol/gr in AT gruoup versus 0.5144 ± 0.29 nmol/gr in GT group, p=0.028).

Conclusion: LDL oxidation was significantly increase after glucocortikoid treatment and atorvastatin therapy was improved this problem in Sprague-Dawley rats.