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Apocynin attenuates cholesterol oxidation product-induced programmed cell death by suppressing NF-κB-mediated cell death process in differentiated PC12 cells.
Neurochem Int. 2015 10; 89:28-39.NI

Abstract

Cholesterol oxidation products are suggested to be involved in neuronal degeneration. Apocynin has demonstrated to have anti-inflammatory and anti-oxidant effects. We assessed the effect of apocynin on the cholesterol oxidation product-induced programmed cell death in neuronal cells using differentiated PC12 cells in relation to NF-κB-mediated cell death process. 7-Ketocholesterol and 25-hydroxycholesterol decreased the levels of Bid and Bcl-2, increased the levels of Bax and p53, and induced loss of the mitochondrial transmembrane potential, release of cytochrome c and activation of caspases (-8, -9 and -3). 7-Ketocholesterol caused an increase in the levels of cytosolic and nuclear NF-κB p65, cytosolic NF-κB p50 and cytosolic phospho-IκB-α, which was inhibited by the addition of 0.5 μM Bay11-7085 (an inhibitor of NF-κB activation). Apocynin attenuated the cholesterol oxidation product-induced changes in the programmed cell death-related protein levels, NF-κB activation, production of reactive oxygen species, and depletion of GSH. The results show that apocynin appears to attenuate the cholesterol oxidation product-induced programmed cell death in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways that are mediated by NF-κB activation. The preventive effect appears to be associated with the inhibitory effect on the production of reactive oxygen species and depletion of GSH.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, and the BK21(plus) Skin Barrier Network Human Resources Development Team, Chung-Ang University, Seoul 156-756, South Korea.Department of Pharmacology, College of Medicine, and the BK21(plus) Skin Barrier Network Human Resources Development Team, Chung-Ang University, Seoul 156-756, South Korea.Department of Pharmacology, College of Medicine, and the BK21(plus) Skin Barrier Network Human Resources Development Team, Chung-Ang University, Seoul 156-756, South Korea. Electronic address: leecs@cau.ac.kr.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26122972

Citation

Lee, Da Hee, et al. "Apocynin Attenuates Cholesterol Oxidation Product-induced Programmed Cell Death By Suppressing NF-κB-mediated Cell Death Process in Differentiated PC12 Cells." Neurochemistry International, vol. 89, 2015, pp. 28-39.
Lee DH, Nam YJ, Lee CS. Apocynin attenuates cholesterol oxidation product-induced programmed cell death by suppressing NF-κB-mediated cell death process in differentiated PC12 cells. Neurochem Int. 2015;89:28-39.
Lee, D. H., Nam, Y. J., & Lee, C. S. (2015). Apocynin attenuates cholesterol oxidation product-induced programmed cell death by suppressing NF-κB-mediated cell death process in differentiated PC12 cells. Neurochemistry International, 89, 28-39. https://doi.org/10.1016/j.neuint.2015.06.012
Lee DH, Nam YJ, Lee CS. Apocynin Attenuates Cholesterol Oxidation Product-induced Programmed Cell Death By Suppressing NF-κB-mediated Cell Death Process in Differentiated PC12 Cells. Neurochem Int. 2015;89:28-39. PubMed PMID: 26122972.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apocynin attenuates cholesterol oxidation product-induced programmed cell death by suppressing NF-κB-mediated cell death process in differentiated PC12 cells. AU - Lee,Da Hee, AU - Nam,Yoon Jeong, AU - Lee,Chung Soo, Y1 - 2015/06/26/ PY - 2015/03/31/received PY - 2015/06/04/revised PY - 2015/06/10/accepted PY - 2015/7/1/entrez PY - 2015/7/1/pubmed PY - 2016/7/5/medline KW - Apocynin KW - Cell protection KW - Cholesterol oxidation products KW - Differentiated PC12 cells KW - NF-κB activation KW - Programmed cell death-related proteins SP - 28 EP - 39 JF - Neurochemistry international JO - Neurochem. Int. VL - 89 N2 - Cholesterol oxidation products are suggested to be involved in neuronal degeneration. Apocynin has demonstrated to have anti-inflammatory and anti-oxidant effects. We assessed the effect of apocynin on the cholesterol oxidation product-induced programmed cell death in neuronal cells using differentiated PC12 cells in relation to NF-κB-mediated cell death process. 7-Ketocholesterol and 25-hydroxycholesterol decreased the levels of Bid and Bcl-2, increased the levels of Bax and p53, and induced loss of the mitochondrial transmembrane potential, release of cytochrome c and activation of caspases (-8, -9 and -3). 7-Ketocholesterol caused an increase in the levels of cytosolic and nuclear NF-κB p65, cytosolic NF-κB p50 and cytosolic phospho-IκB-α, which was inhibited by the addition of 0.5 μM Bay11-7085 (an inhibitor of NF-κB activation). Apocynin attenuated the cholesterol oxidation product-induced changes in the programmed cell death-related protein levels, NF-κB activation, production of reactive oxygen species, and depletion of GSH. The results show that apocynin appears to attenuate the cholesterol oxidation product-induced programmed cell death in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways that are mediated by NF-κB activation. The preventive effect appears to be associated with the inhibitory effect on the production of reactive oxygen species and depletion of GSH. SN - 1872-9754 UR - https://www.unboundmedicine.com/medline/citation/26122972/Apocynin_attenuates_cholesterol_oxidation_product_induced_programmed_cell_death_by_suppressing_NF_κB_mediated_cell_death_process_in_differentiated_PC12_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(15)00096-0 DB - PRIME DP - Unbound Medicine ER -