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

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(CCK8), 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 μmol/L) prevented FA-induced cell death in SH-SY5 Y 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(5 μmol/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(P0.05). Additionally, Icariin inhibited FA-induced cell apoptosis in SH-SY5 Y 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 phosphorylation.     

甲醛与阿尔茨海默病的基础与临床研究进展

越来越多的基础和临床研究证明,甲醛与阿尔茨海默病(AD)可能有因果关系。实验表明,超浓度甲醛可直接损伤神经元或神经化学物质,可使动物或人的认知、记忆、社会交往和情感异常;甚至可以引起神经纤维缠结(NFTS);过多产生老年斑(SP)。AD病理特征性改变几乎都可以见到。甲醛在我国