Zhang Ying, Yong Hui-yuan, Shi Xiao-ting, Zhou Jun, Ma Qian, Lian Qing-quan, Cao Hong, Li Jun
Department of Anesthesiology, Second Affiliated Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Department of Anesthesiology, Second Affiliated Hospital, Wenzhou Medical University, Wenzhou 325027, China. Email:
Zhonghua Yi Xue Za Zhi. 2013 Sep 17;93(35):2826-9.
To explore the effects of curcumin on the expression of high mobility group box1 (HMGB1) , cell viability and morphology in a cellular model of Alzheimer's disease (AD).
Cultured PC12 cells in logarithmic growth phase were divided into 5 groups: normal cell group (A, non-treatment), model control group (B, 20 µmol/L Aβ25-35), curcumin treatment group (C, 20 µmol/L Aβ25-35+1 µmol/L Cur), Aβ25-35+rHMG1 (D, 20 µmol/L Aβ25-35+500 ng/ml HMGB1) and solvent control group (E, 20 µmol/L Aβ25-35+1 µl/ml DMSO). Cell viability was examined by methyl thiazolyl tetrazolium (MTT). And the cellular expression and distribution of HMGB1 were detected by immunofluorescence and Western blot 24 hours later.
Compared with group A, the levels of cell viability in groups B, D and E significantly declined (0.76 ± 0.06, 0.63 ± 0.02, 0.75 ± 0.03 vs 1.22 ± 0.06, P < 0.05) while the expression of HMGB1 increased (1.19 ± 0.14, 1.12 ± 0.16, 1.16 ± 0.09 vs 0.85 ± 0.04, P < 0.05). Compared with group B, cell viability in group C significantly increased by 33% (1.01 ± 0.05, P < 0.05) while the expression of HMGB1 declined by 31% (0.78 ± 0.03, P < 0.05). A larger amount of extracellular HMGB1 was released in group B compared with group A. And the extracellular release of HMGB1 declined less in group C versus group B.
Curcumin may reduce Aβ25-35-induced cytotoxicity through a down-regulated expression of HMGB1 and an inhibition of extracellular release of HMGB1 in PC12 cell.
探讨姜黄素对阿尔茨海默病（AD）细胞模型中高迁移率族蛋白B1（HMGB1）表达、细胞活力及细胞形态的影响。
将对数生长期的PC12细胞分为5组：正常细胞组（A组，未处理）、模型对照组（B组，20 μmol/L Aβ25 - 35）、姜黄素处理组（C组，20 μmol/L Aβ25 - 35 + 1 μmol/L姜黄素）、Aβ25 - 35 + rHMG1组（D组，20 μmol/L Aβ25 - 35 + 500 ng/ml HMGB1）和溶剂对照组（E组，20 μmol/L Aβ25 - 35 + 1 μl/ml二甲基亚砜）。采用噻唑蓝（MTT）法检测细胞活力。24小时后，通过免疫荧光和蛋白质印迹法检测HMGB1的细胞表达及分布情况。
与A组相比，B组、D组和E组细胞活力水平显著下降（0.76±0.06、0.63±0.02、0.75±0.03 vs 1.22±0.06，P<0.05），而HMGB1表达增加（1.19±0.14、1.12±0.16、1.16±0.09 vs 0.85±0.04，P<0.05）。与B组相比，C组细胞活力显著增加33%（1.01±0.05，P<0.05），而HMGB1表达下降31%（0.78±0.03，P<0.05）。与A组相比，B组释放到细胞外的HMGB1量更多。与B组相比，C组细胞外HMGB1的释放减少幅度较小。
姜黄素可能通过下调PC12细胞中HMGB1的表达并抑制HMGB1的细胞外释放，减轻Aβ25 - 35诱导的细胞毒性。
