Taxifolin reduces the cholesterol oxidation product-induced neuronal apoptosis by suppressing the Akt and NF-kappa B activation-mediated cell death
- Authors
- Kim, Arum; Nam, Yoon Jeong; Lee, Chung Soo
- Issue Date
- Sep-2017
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- Taxifolin; Cholesterol oxidation products; Akt and NF-kappa B; Apoptosis-related proteins; Cell protection
- Citation
- BRAIN RESEARCH BULLETIN, v.134, pp 63 - 71
- Pages
- 9
- Journal Title
- BRAIN RESEARCH BULLETIN
- Volume
- 134
- Start Page
- 63
- End Page
- 71
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/45522
- DOI
- 10.1016/j.brainresbull.017.07.008
- ISSN
- 0361-9230
1873-2747
- 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-kappa B p65, cytosolic NF-kappa B p50 and cytosolic phosphorylated-I kappa B-alpha 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-kappa B, 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-kappa B activation-mediated cell death. The suppressive effect appears to be attributed to the inhibition of reactive oxygen species production and GSH depletion.
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