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, a...

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Published inChinese journal of integrative medicine Vol. 22; no. 6; pp. 430 - 437
Main Author 宋宜祥 苗君叶 强敏 赫荣乔 王学美 黎巍威
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.06.2016
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ISSN1672-0415
1993-0402
DOI10.1007/s11655-015-2116-3

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Abstract 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.
AbstractList 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.
To investigate the neuroprotective effects of icariin on formaldehyde (FA)-treated human neuroblastoma SH-SY5Y cells and the possible mechanisms involved. 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. 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-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 (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 (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. Icariin protects SH-SY5Y cells from FA-induced injury poßsibly through the inhibition of GSK-3β-mediated 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 (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 µmol/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 (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 ( 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 poßsibly through the inhibition of GSK-3β-mediated Tau phosphorylation.
Author 宋宜祥 苗君叶 强敏 赫荣乔 王学美 黎巍威
AuthorAffiliation Integrated Laboratory of Chinese and Western Medicine, Peking University First Hospital, Beijing (100034), China State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing (100101), China
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Keywords Tau phosphorylation
glycogen synthase kinase 3 beta
icariin
formaldehyde
neuroprotection
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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.
icariin, formaldehyde, Tau phosphorylation, glycogen synthase kinase 3 beta, neuroprotection
PMID 26589607
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PublicationTitle Chinese journal of integrative medicine
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Snippet Objective: To investigate the neuroprotective effects of icariin on formaldehyde (FA)-treated human neuroblastoma SH-SY5Y cells and the possible mechanisms...
Objective To investigate the neuroprotective effects of icariin on formaldehyde (FA)-treated human neuroblastoma SH-SY5Y cells and the possible mechanisms...
To investigate the neuroprotective effects of icariin on formaldehyde (FA)-treated human neuroblastoma SH-SY5Y cells and the possible mechanisms involved....
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crossref
springer
chongqing
SourceType Index Database
Enrichment Source
Publisher
StartPage 430
SubjectTerms Blotting, Western
Cell Death - drug effects
Cell Line, Tumor
Cell Shape - drug effects
Cell Survival - drug effects
DNA Fragmentation - drug effects
Flavonoids - pharmacology
Formaldehyde
Glycogen Synthase Kinase 3 beta - antagonists & inhibitors
Glycogen Synthase Kinase 3 beta - metabolism
Humans
Medicine
Medicine & Public Health
Neuroprotective Agents - pharmacology
Original Article
Phosphorylation - drug effects
SH-SY5Y细胞
tau Proteins - metabolism
tau蛋白
半数致死剂量
淫羊藿苷
激光共聚焦显微镜
甲醛
细胞损伤
蛋白磷酸化
Title Icariin Protects SH-SY5Y Cells from Formaldehyde-Induced Injury through Suppression of Tau Phosphorylation
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https://link.springer.com/article/10.1007/s11655-015-2116-3
https://www.ncbi.nlm.nih.gov/pubmed/26589607
Volume 22
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