姜黄素抑制β淀粉样蛋白致小胶质瘤细胞神经炎症反应

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Abstract Objective: To explore the relationship between high mobility group box1 (HMGB1) and inflammatory response of the receptor for advanced glycation end product (RAGE) with inflammation model of Alzheimer’s disease (AD) selected Aβ25-35-induced BV2 cells for 24 hours later, to further investigate the effects of curcumin on expression of HMGB1, RAGE, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) in Aβ25-35-induced BV2 cells. Methods: Cultured BV2 cells in logarithmic growth phase were divided into 4 groups: control group (group A, non-treament), model Aβ25-35 group (group B, 40 µmol/L Aβ25-35, 24 h), Aβ25-35+anti-RAGE antibody group (group C, 10 µmol/L anti-RAGE antibody 1 h before+40 µmol/L Aβ25-35, 24 h) and Aβ25-35+curcumin treatment group (group D, 8 µmol/L curcumin 1 h before+40 µmol/L Aβ25-35, 24 h). The morphological character of BV2 cells was observed 24 hours later and cells viability was examined by CCK8, the level expression of HMGB1, NF-κB, RAGE in cells were detected by western blotting. The level secretion of HMGB1, IL-1β, TNF-α were detected by ELISA 24 hours later. Results: Compared with group A, the cell viability in group B and C were significantly declined and the level of HMGB1 protein expression in cells was significantly increased (P<0.05), the expression of total NF-κB were significantly increased (P<0.05), IL-1β and TNF-α in supernatant were significantly increased (P<0.05). Compared with group B and C, the cell viability, the level of HMGB1 and NF-κB protein expression in cells significantly declined, HMGB1/IL-1β and TNF-α in supernatant significantly declined in group D (P<0.05). Conclusion: Curcumin may reduce Aβ25-35-induced neuroinﬂammation in BV2 cells through inhibiting HMGB1 expression/extracellular released and inhibition NF-κB pathway, partly correlated with RAGE expression down-regulatd.

Key words： Alzheimer’s disease curcumin amyloid beta-protein BV2 cells high mobility group proteins receptor for advanced glycation end product

Received: 31 March 2016

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https://xb.wmu.edu.cn/EN/ OR https://xb.wmu.edu.cn/EN/Y2017/V47/I2/85

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