Aluminum-induced "mixed" cell death in mice cerebral tissue and potential intervention.

摘要: The brain is one of organs vulnerable to aluminum insult. Aluminum toxicity involved in neurobehavioral deficit, neuronal cell dysfunction, and death. aim this study are as follows: (1) evaluate the repairing efficiency Necrostatin-1 (Nec-1), a death inhibitor, Z-VAD-FMK, pan-caspase on Al-induced deficit death, order evidence inducing ability aluminum, (2) primarily explore possibility treating loss-related disease, such Alzheimer's with Nec-1 Z-VAD dementia animal model. We found Z-VAD-FMK alone or combination could reduce aluminum-induced learning memory impairment mice. Pathohistological results indicated that can decrease cell. In addition, some death-associated proteins signal pathway were inhibited by Al-exposed conclusions, repair injury induced Furthermore, was more obvious function compared Z-VAD-FMK. morphological amounts dead cell, effects significant at higher doses. effect stronger than though their mechanism different. them had strongest effect. Our evidenced necroptosis apoptosis existing model suggested potential therapeutic neurodegenerative diseases.