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


CONCLUSIONS
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.
Shen
Yu-Xian
YX
Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, China. shenyuxi@mail.hf.ah.cn
Wei
Wei
W
Xu
Shu-Yun
SY
D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects* / Q000473:pathology; D004347:Drug Interactions; D005333:Fetus; D016166:Free Radical Scavengers / Q000494:pharmacology; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008550:Melatonin / Q000494:pharmacology*; D009474:Neurons / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D016229:Amyloid beta-Peptides; D016166:Free Radical Scavengers; D018696:Neuroprotective Agents; C439320:amyloid beta-protein (25-36); D007770:L-Lactate Dehydrogenase; D008550:Melatonin