RESUMO
Objective To investigate the role of HIV-1 envelope protein gp120 in cognitive im-pairment induced by neuronal damage. Methods Western blot and immunofluorescence assay were used to detect microglia activation, inflammatory factor expression and neuronal damage after gp120 treatment. Neu-ronal damage and neurocognitive performance in gp120-transgenic mice were evaluated using immunohisto-chemical staining and behavioral analysis, respectively. Results In vivo and in vitro experiments showed that HIV-1 gp120 significantly induced the expression of caspase-1 and IL-1β, and indirectly caused neuro-nal synaptic shortening and neuronal damage (P<0. 05). Compared with wild-type mice, gp120-transgenic mice showed significant cortical and hippocampal glial activation, neuronal loss, dendritic damage and neu-rocognitive disorders. Conclusions HIV-1 gp120 might cause neuronal damage through activating the re-lease of inflammatory factor by microglia and involve in neurocognitive impairment.
RESUMO
Objective@#To investigate the role of HIV-1 envelope protein gp120 in cognitive impairment induced by neuronal damage.@*Methods@#Western blot and immunofluorescence assay were used to detect microglia activation, inflammatory factor expression and neuronal damage after gp120 treatment. Neuronal damage and neurocognitive performance in gp120-transgenic mice were evaluated using immunohistochemical staining and behavioral analysis, respectively.@*Results@#In vivo and in vitro experiments showed that HIV-1 gp120 significantly induced the expression of caspase-1 and IL-1β, and indirectly caused neuronal synaptic shortening and neuronal damage (P<0.05). Compared with wild-type mice, gp120-transgenic mice showed significant cortical and hippocampal glial activation, neuronal loss, dendritic damage and neurocognitive disorders.@*Conclusions@#HIV-1 gp120 might cause neuronal damage through activating the release of inflammatory factor by microglia and involve in neurocognitive impairment.