Protective effects of melatonin on cortico-hippocampal neurotoxicity induced by amyloid beta-peptide 25-35.

AIM: To study the effects of melatonin on primary rat cortico-hippocampal
neurotoxicity induced by amyloid beta-peptide 25-35.
METHODS: The neuronal morphology was observed by phase-contrast microscopy. The
neurotoxicity was quantitatively estimated by measuring lactate dehydrogenase
(LDH) released into the culture medium from the damaged neurons. The neuronal
metabolic state was quantified by the reduction of
3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT).
RESULTS: Treatment of primary rat cortico-hippocampal neurons with amyloid
beta-peptide 25-35 (20 micromol/L) for 24 h caused a significant decrease in
neurocyte viability (P < 0.01, compared with control). Melatonin (1 or 10
micromol/L) reduced the neurotoxicity induced by amyloid beta-peptide 25-35.
CONCLUSION: Amyloid beta-peptide 25-35 could exert direct cytotoxicity on rat
cortico-hippocampal neurocytes and melatonin concentration-dependently rescued
cultured neurons from exposure to amyloid beta-peptide 25-35 induced injury.