[Protective effect of curcumin against Aβ25-35-induced neurotoxicity in differentiated PC12 cells].
Ying Zhang, Hui-yuan Yong, Xiao-ting Shi, Jun Ma Zhou, Qian Ma, Qingquan Lian, Hong Cao, Jun Li
Abstract
Ying Zhang, Hui-yuan Yong, Xiao-ting Shi, Jun Ma Zhou, Qian Ma, Qingquan Lian, Hong Cao, Jun Li
Abstract
OBJECTIVE: 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). METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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OBJECTIVE: 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). METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Key concepts: HMGB1, Viability assay, Extracellular, Curcumin, Western blot, Chemistry, Andrology, Molecular biology