Icariin Protects SH-SY5Y Cells from Formaldehyde-Induced Injury through Suppression of Tau Phosphorylation  

作　　者：宋宜祥 苗君叶 强敏 赫荣乔 王学美 黎巍威 

机构地区：[1]Integrated Laboratory of Chinese and Western Medicine, Peking University First Hospital [2]State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences

出　　处：《Chinese Journal of Integrative Medicine》2016年第6期430-437,共8页中国结合医学杂志（英文版）

基　　金：Supported by the National Natural Science Foundation of China(No.81102683 and No.81173369);the Doctoral Fellowships of Ministry of Education of China(No.20120001110105 and No.20110001120055);Beijing Natural Science Foundation(No.7132210)

摘　　要：Objective： To investigate the neuroprotective effects of icariin on formaldehyde （FA）-treated human neuroblastoma SH-SY5Y cells and the possible mechanisms involved. Methods： SH-SY5Y cells were divided into FA treatment group, FA treatment group with icariin, and the control group. Cell viability, apoptosis, and morphological changes were determined by cell counting kit-8 （CCK 8）, flow cytometry, and confocal microscopy, respectively. The phosphorylation of Tau protein was examined by western blotting. Results： FA showed a half lethal dose （LD50） of 0.3 mmol/L in SH-SY5Y cells under the experimental conditions. Icariin （1-10 μ mol/L） prevented FA-induced cell death in SH-SY5Y cells in a dose-dependent manner, with the optimal effect observed at 5 μmol/L. After FA treatment, the absorbance in FA group was 1.31±0.05, while in the group of icariin （5μmol/L） was 1.63±0.05. Examination of cell morphology by confocal microscopy demonstrated that 5 μmol/L icariin significantly attenuated FA-induced cell injury （P〈0.05）. Additionally, icariin inhibited FA-induced cell apoptosis in SH-SY5Y cells. Results from western blotting showed that icariin suppressed FA-induced phosphorylation at Thr 181 and Ser 396 of Tau protein, while having no effect on the expression of the total Tau protein level. Furthermore, FA activated Tau kinase glycogen synthase kinase 3 beta （GSK-3β） by enhancement of Y216 phosphorylation, but icariin reduced Y216 phosphorylation and increased Ser 9 phosphorylation. Conclusion： Icariin protects SH-SY5Y cells from FA-induced injury possibly through the inhibition of GSK-3β -mediated Tau phosphoryiation.Objective： To investigate the neuroprotective effects of icariin on formaldehyde （FA）-treated human neuroblastoma SH-SY5Y cells and the possible mechanisms involved. Methods： SH-SY5Y cells were divided into FA treatment group, FA treatment group with icariin, and the control group. Cell viability, apoptosis, and morphological changes were determined by cell counting kit-8 （CCK 8）, flow cytometry, and confocal microscopy, respectively. The phosphorylation of Tau protein was examined by western blotting. Results： FA showed a half lethal dose （LD50） of 0.3 mmol/L in SH-SY5Y cells under the experimental conditions. Icariin （1-10 μ mol/L） prevented FA-induced cell death in SH-SY5Y cells in a dose-dependent manner, with the optimal effect observed at 5 μmol/L. After FA treatment, the absorbance in FA group was 1.31±0.05, while in the group of icariin （5μmol/L） was 1.63±0.05. Examination of cell morphology by confocal microscopy demonstrated that 5 μmol/L icariin significantly attenuated FA-induced cell injury （P〈0.05）. Additionally, icariin inhibited FA-induced cell apoptosis in SH-SY5Y cells. Results from western blotting showed that icariin suppressed FA-induced phosphorylation at Thr 181 and Ser 396 of Tau protein, while having no effect on the expression of the total Tau protein level. Furthermore, FA activated Tau kinase glycogen synthase kinase 3 beta （GSK-3β） by enhancement of Y216 phosphorylation, but icariin reduced Y216 phosphorylation and increased Ser 9 phosphorylation. Conclusion： Icariin protects SH-SY5Y cells from FA-induced injury possibly through the inhibition of GSK-3β -mediated Tau phosphoryiation.

关 键 词：ICARIIN FORMALDEHYDE Tau phosphorylation glycogen synthase kinase 3 beta NEUROPROTECTION 

分 类 号：R285[医药卫生—中药学]