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.

A model of acute lung injury was reproduced by intravenous injection of endotoxin (700?g / kg) to rabbits. It had been found that the rabbits were in the state of shock, with leukopenia and thrombocytopenia, increased 6 -keto-PGF1? and TXB2, decreased serum ACE and increased permeability of the pulmonary capillaries. Granulocyte sequestration and disturbance in pulmonary microcirculation were found in lungs. A series of changes in epithelial and endothelial cells were also found in both lungs. It was obviously proved that PGE1 had some therapeutic effects in acute lung injury induced by E. coli endotoxin.