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 in | Chinese journal of integrative medicine Vol. 22; no. 6; pp. 430 - 437 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.06.2016
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Subjects | |
Online Access | Get full text |
ISSN | 1672-0415 1993-0402 |
DOI | 10.1007/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. |
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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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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26589607$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1002_ptr_8344 crossref_primary_10_1002_ardp_202400721 crossref_primary_10_3390_pharmaceutics15061568 crossref_primary_10_1080_1028415X_2022_2158931 crossref_primary_10_3390_ijms20205090 crossref_primary_10_1096_fj_201701386 crossref_primary_10_1155_2019_7940808 crossref_primary_10_1155_2022_5981353 crossref_primary_10_1016_j_ejphar_2018_10_006 crossref_primary_10_1016_j_ijbiomac_2024_130580 |
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Keywords | Tau phosphorylation glycogen synthase kinase 3 beta icariin formaldehyde neuroprotection |
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Notes | 11-4928/R 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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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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