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Updated: Oct 2, 2026
A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
Published on: May 22, 2018
Protective effects of melatonin on cortico-hippocampal neurotoxicity induced by amyloid beta-peptide 25-35
Yu-Xian Shen1, Wei Wei, Shu-Yun Xu
1Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, China. shenyuxi@mail.hf.ah.cn
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.
