Abstract:

 AIM: To investigate the changes of high mobility group box 1 protein (HMGB1) and receptor of advanced glycation (RAGE) in neurons damaged by β-amyloid 25-35 (Aβ _25-35).  METHODS: Primary hippocampal neurons were chosen and cultured 7 days with different concentrations of Aβ _25-35. CCK-8 test was used to detect cell viability for determining drug concentration and reaction time. Primary hippocampal neurons were then divided into two groups, i.e. the normal cell group (group C) and the injury group (group I). Neuronal morphology and Western blot technique were applied to detect the expression level of HMGB1 in cytoplasm and nucleus as well as RAGE and NF-κB in the cytoplasm. The quantity of HMGB1, IL-1β and TNF-α in supernatant of neurons was detected by ELISA.RESULTS:Neuron injured model was determined with Aβ25-35 concentration at 25 μmol/L and reaction time for 24 h by CCK-8 test. Morphology showed neurons decreased significantly and most of them in aggregation state in group I. Western blot showed the expression level of HMGB1 in cytoplasm was significantly lower than that in group C (1.596±0.189 vs. 0.146±0.043, P<0.05), while HMGB1 in cell nucleus was higher than that in group C (0.934±0.145 vs. 1.370±0.354, P<0.05), the expression level of RAGE and NF-κB in cytoplasm were higher in group I than those in group C (0.962±0.180 vs. 1.253±0.254, 0.825±0.116 vs. 1.023±0.150, P<0.05). ELISA showed the quantity of HMGB1, IL-1β and TNF-α in supernatant were significantly higher in group I than those in group C (P<0.05). CONCLUSION:Signal proteins of HMGB1, RAGE and inflammatory factors such as IL-1β and TNF-α were obviously increased in Aβ25-35 injured neurons; HMGB1 might be involved in Aβ _25-35 injured neuronal inflammation through RAGE/ NF-κB inflammatory pathway.

Key words: Alzheimer's disease, β-amyloid protein, neuron, high mobility group protein 1