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Taxifolin reduces the cholesterol oxidation product-induced neuronal apoptosis by suppressing the Akt and NF-κB activation-mediated cell death.
Brain Res Bull. 2017 Sep; 134:63-71.BR

Abstract

The taxifolin effect on the cholesterol oxidation product-induced neuronal apoptosis was investigated using differentiated PC12 cells and human neuroblastoma SH-SY5Y cells. 7-ketocholesterol induced phosphorylation of Akt, and increase in the levels of cytosolic and nuclear NF-κB p65, cytosolic NF-κB p50 and cytosolic phosphorylated-IκB-α in PC12 cells. The cholesterol oxidation products also induced a decrease in the levels of Bid and Bcl-2, increase in the levels of p53 and Bax, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), production of reactive oxygen species, depletion of GSH and cell death in both cell lines. Taxifolin, N-acetylcysteine, trolox, Akt inhibitor and Bay11-7085 attenuated the cholesterol oxidation product-induced changes in the apoptosis-related protein levels, activation of the Akt and NF-κB, reactive oxygen species production, GSH depletion and cell death. These results show that taxifolin may reduce the cholesterol oxidation product-induced neuronal apoptosis by suppressing the Akt and NF-κB activation-mediated cell death. The suppressive effect appears to be attributed to the inhibition of reactive oxygen species production and GSH depletion.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, and the BK21plus Skin Barrier Network Human Resources Development Team, Chung-Ang University, Seoul 156-756, Republic of Korea.Department of Pharmacology, College of Medicine, and the BK21plus Skin Barrier Network Human Resources Development Team, Chung-Ang University, Seoul 156-756, Republic of Korea.Department of Pharmacology, College of Medicine, and the BK21plus Skin Barrier Network Human Resources Development Team, Chung-Ang University, Seoul 156-756, Republic of Korea. Electronic address: leecs@cau.ac.kr.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28710022

Citation

Kim, Arum, et al. "Taxifolin Reduces the Cholesterol Oxidation Product-induced Neuronal Apoptosis By Suppressing the Akt and NF-κB Activation-mediated Cell Death." Brain Research Bulletin, vol. 134, 2017, pp. 63-71.
Kim A, Nam YJ, Lee CS. Taxifolin reduces the cholesterol oxidation product-induced neuronal apoptosis by suppressing the Akt and NF-κB activation-mediated cell death. Brain Res Bull. 2017;134:63-71.
Kim, A., Nam, Y. J., & Lee, C. S. (2017). Taxifolin reduces the cholesterol oxidation product-induced neuronal apoptosis by suppressing the Akt and NF-κB activation-mediated cell death. Brain Research Bulletin, 134, 63-71. https://doi.org/10.1016/j.brainresbull.2017.07.008
Kim A, Nam YJ, Lee CS. Taxifolin Reduces the Cholesterol Oxidation Product-induced Neuronal Apoptosis By Suppressing the Akt and NF-κB Activation-mediated Cell Death. Brain Res Bull. 2017;134:63-71. PubMed PMID: 28710022.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Taxifolin reduces the cholesterol oxidation product-induced neuronal apoptosis by suppressing the Akt and NF-κB activation-mediated cell death. AU - Kim,Arum, AU - Nam,Yoon Jeong, AU - Lee,Chung Soo, Y1 - 2017/07/11/ PY - 2017/04/16/received PY - 2017/07/06/revised PY - 2017/07/07/accepted PY - 2017/7/16/pubmed PY - 2018/5/8/medline PY - 2017/7/16/entrez KW - Akt and NF-κB KW - Apoptosis-related proteins KW - Cell protection KW - Cholesterol oxidation products KW - Taxifolin SP - 63 EP - 71 JF - Brain research bulletin JO - Brain Res. Bull. VL - 134 N2 - The taxifolin effect on the cholesterol oxidation product-induced neuronal apoptosis was investigated using differentiated PC12 cells and human neuroblastoma SH-SY5Y cells. 7-ketocholesterol induced phosphorylation of Akt, and increase in the levels of cytosolic and nuclear NF-κB p65, cytosolic NF-κB p50 and cytosolic phosphorylated-IκB-α in PC12 cells. The cholesterol oxidation products also induced a decrease in the levels of Bid and Bcl-2, increase in the levels of p53 and Bax, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), production of reactive oxygen species, depletion of GSH and cell death in both cell lines. Taxifolin, N-acetylcysteine, trolox, Akt inhibitor and Bay11-7085 attenuated the cholesterol oxidation product-induced changes in the apoptosis-related protein levels, activation of the Akt and NF-κB, reactive oxygen species production, GSH depletion and cell death. These results show that taxifolin may reduce the cholesterol oxidation product-induced neuronal apoptosis by suppressing the Akt and NF-κB activation-mediated cell death. The suppressive effect appears to be attributed to the inhibition of reactive oxygen species production and GSH depletion. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/28710022/Taxifolin_reduces_the_cholesterol_oxidation_product_induced_neuronal_apoptosis_by_suppressing_the_Akt_and_NF_κB_activation_mediated_cell_death_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(17)30227-7 DB - PRIME DP - Unbound Medicine ER -