RESUMO
AIM: To investigate the effects of curcumin (Cur) on the expression of High mobility group box 1 protein (HMGB1), interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α) in amyloid-β(Aβ)-induced primary rat microglial cells.METHODS: Microglia were derived from the cerebral cortices of postnatal rat brains.The cells were i-dentified by immunocytochemistry using mouse anti rat Iba-1 monoclonal antibody.A cell model using primary rat microgli-al cells incubated with Aβ25-35 as an inflammation model of Alzheimer’s disease (AD) was set up.The morphological char-acters of primary rat microglial cells were observed.The concentration of Aβ25-35 and the treatment concentration of curcumin were selected by CCK-8 assay.Cultured primary rat microglial cells were divided into 5 groups: normal cell group, Aβ25-35 group, Cur group, Aβ25-35 +Cur group and Aβ25-35 +DMSO group.The expression of HMGB1, NF-κB, and receptor for advanced glycation end products (RAGE) was detected by Western blot.The levels of HMGB1, IL-1β, and TNF-αin the culture supernatant were measured by ELISA.RESULTS: The purity of primary microglias determined by Iba-1 immuno-fluorescence was more than 95%.The protein levels of HMGB1, RAGE and NF-κB were significantly increased after Aβ25-35 stimulation.After treatment with Cur, the protein levels of HMGB1, RAGE and NF-κB were significantly decreased (P <0.05).The levels of HMGB1, IL-1βand TNF-αin the supernatant were significantly increased after Aβ25-35 stimula-tion.Cur significantly decreased the level of HMGB1, IL-1βand TNF-αin the supernatant.CONCLUSION: Curcumin significantly inhibits neuroinflammation stimulated by Aβ25-35 in primary rat microglial cells.