Effect of testosterone on the cereble cortex Bcl-2 expression and oxidative stress in a rat model of vascular dementia

Document Type : Original Article

Authors

1 Medical Physiology Department1, Mansoura Faculty of Medicine, Egypt, Medical Physiology Department2, College of Medicine, King Khalid University, KSA

2 Medical Physiology Department, Mansoura Faculty of Medicine, Egypt,

Abstract

Objectives to investigate the effect of testosterone on the cerebral cortex Bcl-2 expression and oxidative stress in a rat model of vascular dementia (VD). Methods Forty-eight Sprague-Dawley adult male rats were divided into four groups (n=12, each) as follows (i) untreated control, (ii) rats exposed to surgical permanent bilateral occlusion of the common carotid arteries (BCCAO) leading to chronic cerebral hypoperfusion, (iii) rats exposed to BCCAO then received testosterone (0.5 mg/ kg S.C., three times/ week, S.C.) (BCCAO + Tes) for 4 weeks and (iv) rats exposed to BCCAO then received donepezil (3 mg/kg/ day; i.p.) (BCCAO + DON) for 4 weeks. Levels of acetylcholine and norepinephrine in the cerebral cortex were measured. Furthermore, the expression of Bcl-2 in the cerebral cortex and malondialdehyde (MDA), non-enzymatic (reduced glutathione, GSH) and enzymatic [superoxide dismutase (SOD) and catalase (CAT)] anti-oxidants were determined. Histopathological studies of the cerebral cortex were performed. Results BCCAO decreased the expression of Bcl-2 as well as the central level of acetylcholine and norepinephrine as compared to control rats. Also, increased the cerebral cortex level of MDA and decreased the enzymatic and non-enzymatic antioxidant. Treatment with testosterone and donepezil increased acetylcholine and norepinephrine significantly when compared with BCCAO rats. Testosterone significantly increased the expression of Bcl-2 and antioxidant system with significant reduction in MDA. Conclusion Testosterone might employ neuroprotective effects through increasing the expression of Bcl-2 as well as ameliorating the oxidative stress induced by BCCAO in rat model of DA.

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