Publications of Faculty of Medicine: EFFECTS OF GLIMEPIRIDE (AMARYL) ON BIOGENIC AMINES CONTENT IN DIFFERENT AREAS IN THE BRAIN OF ADULT DIABETIC MALE ALBINO MICE/RATS : Abstract

Title:
EFFECTS OF GLIMEPIRIDE (AMARYL) ON BIOGENIC AMINES CONTENT IN DIFFERENT AREAS IN THE BRAIN OF ADULT DIABETIC MALE ALBINO MICE/RATS
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Abstract:

This work was conducted to investigate the effect of glimepiride on the brain chemical neurotransmitters norepinephrine (NE), serotonine (5- HT), gamma-aminobutyric acid (GABA) and dopamine (DA) in different brain areas namely cerebral cortex (C.C.), thalamus/ hypothalamus (TH), midbrain (M.B.) and cerebellum (C.) in streptozotocin (STZ) induced diabetes and to study the effect of Vit E separately and concomitantly with glimepiride on the previous neurotransmitters. In diabetes induced experimentally in rats by streptozotocin (STZ) (50 mg/kg I.P) results of the present work showed significant elevation of NE level (P < 0.05) in CC, TH, and GABA in all tested brain areas and significant reduction of DA and 5HT levels (P<0.05) in all tested brain areas compared with normal rats. In diabetic group treated with glimepiride (0.1 mg/kg orally), results of the present work showed significant elevation of GABA levels, reduction of DA levels (P<0.05) in all tested brain areas. In diabetic rats treated with Vit, E (0.1 mg/kg orally) there were non significant changes (P >0.05) of GABA, DA, NE and 5HT levels (P > 0.05) in all tested brain areas compared with diabetic non treated rats. Concomitant administrations of glimepiride (0.1 mg/kg orally) and Vit. E (0.1 mg/kg orally) showed significant reduction of GABA, significant elevation of 5HT levels (P<0.05) in all tested brain areas with significant reduction of NE level (P<0.05) in CC, TH.In conclusion: Diabetes may induce brain damage due to oxidative stress and hyperglycemia by disturbing the turnover rate of monoamines and GABA, glimepiride minimize these brain effects, moreover, coadministration •of Vit. E and glimepiride correct hypergleyemia and increase brain protection against hyperglycemia by correcting the disturbed turnover rate of monoamines and GABA.