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Quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside attenuates cholesterol oxidation product-induced apoptosis by suppressing NF-κB-mediated cell death process in differentiated PC12 cells.
Naunyn Schmiedebergs Arch Pharmacol. 2015 Aug; 388(8):869-81.NS

Abstract

Cholesterol oxidation products are suggested to be involved in neuronal cell degeneration. We examined the preventive effect of quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside (QGR), a quercetin derivative, on the cholesterol oxidation product-induced neuronal cell death using differentiated PC12 cells in relation to nuclear factor (NF)-κB-mediated apoptotic process. 7-Ketocholesterol and 25-hydroxycholesterol induced a decrease in the levels of BH3 interacting-domain death agonist (Bid) and B cell lymphoma 2 (Bcl-2), increase in the levels of Bcl-2-associated X protein (Bax) and p53, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases, and cleavage of poly(ADP-ribose) polymerase 1 (PARP-1). 7-Ketocholesterol induced increase in cytosolic and nuclear NF-κB p65, nuclear phospho-NF-κB p65, cytosolic NF-κB p50, and cytosolic phospho-IκB-α levels. The addition of QGR, N-acetyl cysteine, or Bay 11-7085 attenuated the cholesterol oxidation product-induced changes in the apoptosis-related protein levels, activation of NF-κB, formation of reactive oxygen species, depletion of glutathione (GSH), nuclear damage, and cell death. The results show that QGR may attenuate the cholesterol oxidation product-induced apoptosis in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways that is mediated by NF-κB activation. The preventive effect appears to be associated with the inhibitory effect on the formation of reactive oxygen species and depletion of GSH.

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, South Korea.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25845326

Citation

Lee, Da Hee, et al. "Quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside Attenuates Cholesterol Oxidation Product-induced Apoptosis By Suppressing NF-κB-mediated Cell Death Process in Differentiated PC12 Cells." Naunyn-Schmiedeberg's Archives of Pharmacology, vol. 388, no. 8, 2015, pp. 869-81.
Lee DH, Nam YJ, Lee CS. Quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside attenuates cholesterol oxidation product-induced apoptosis by suppressing NF-κB-mediated cell death process in differentiated PC12 cells. Naunyn Schmiedebergs Arch Pharmacol. 2015;388(8):869-81.
Lee, D. H., Nam, Y. J., & Lee, C. S. (2015). Quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside attenuates cholesterol oxidation product-induced apoptosis by suppressing NF-κB-mediated cell death process in differentiated PC12 cells. Naunyn-Schmiedeberg's Archives of Pharmacology, 388(8), 869-81. https://doi.org/10.1007/s00210-015-1120-7
Lee DH, Nam YJ, Lee CS. Quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside Attenuates Cholesterol Oxidation Product-induced Apoptosis By Suppressing NF-κB-mediated Cell Death Process in Differentiated PC12 Cells. Naunyn Schmiedebergs Arch Pharmacol. 2015;388(8):869-81. PubMed PMID: 25845326.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside attenuates cholesterol oxidation product-induced apoptosis 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 - 2015/04/07/ PY - 2015/01/06/received PY - 2015/03/26/accepted PY - 2015/4/8/entrez PY - 2015/4/8/pubmed PY - 2016/4/1/medline SP - 869 EP - 81 JF - Naunyn-Schmiedeberg's archives of pharmacology JO - Naunyn Schmiedebergs Arch. Pharmacol. VL - 388 IS - 8 N2 - Cholesterol oxidation products are suggested to be involved in neuronal cell degeneration. We examined the preventive effect of quercetin-3-O-(2″-galloyl)-α-L-rhamnopyranoside (QGR), a quercetin derivative, on the cholesterol oxidation product-induced neuronal cell death using differentiated PC12 cells in relation to nuclear factor (NF)-κB-mediated apoptotic process. 7-Ketocholesterol and 25-hydroxycholesterol induced a decrease in the levels of BH3 interacting-domain death agonist (Bid) and B cell lymphoma 2 (Bcl-2), increase in the levels of Bcl-2-associated X protein (Bax) and p53, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases, and cleavage of poly(ADP-ribose) polymerase 1 (PARP-1). 7-Ketocholesterol induced increase in cytosolic and nuclear NF-κB p65, nuclear phospho-NF-κB p65, cytosolic NF-κB p50, and cytosolic phospho-IκB-α levels. The addition of QGR, N-acetyl cysteine, or Bay 11-7085 attenuated the cholesterol oxidation product-induced changes in the apoptosis-related protein levels, activation of NF-κB, formation of reactive oxygen species, depletion of glutathione (GSH), nuclear damage, and cell death. The results show that QGR may attenuate the cholesterol oxidation product-induced apoptosis in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways that is mediated by NF-κB activation. The preventive effect appears to be associated with the inhibitory effect on the formation of reactive oxygen species and depletion of GSH. SN - 1432-1912 UR - https://www.unboundmedicine.com/medline/citation/25845326/Quercetin_3_O__2″_galloyl__α_L_rhamnopyranoside_attenuates_cholesterol_oxidation_product_induced_apoptosis_by_suppressing_NF_κB_mediated_cell_death_process_in_differentiated_PC12_cells_ L2 - https://dx.doi.org/10.1007/s00210-015-1120-7 DB - PRIME DP - Unbound Medicine ER -