{'fraction_non_alphanumeric': 0.045172719220549155, 'fraction_numerical': 0.0354295837023915, 'mean_word_length': 5.277777777777778, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
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.