https://scholars.lib.ntu.edu.tw/handle/123456789/508560
標題: | Inhibition of NADPH oxidase-related oxidative stress-triggered signaling by honokiol suppresses high glucose-induced human endothelial cell apoptosis | 作者: | Sheu M.L. CHIH-KANG CHIANG KEH-SUNG TSAI Ho F.M. TE-I WENG Wu H.Y. Liu S.H. |
公開日期: | 2008 | 卷: | 44 | 期: | 12 | 起(迄)頁: | 2043-2050 | 來源出版物: | Free Radical Biology and Medicine | 摘要: | Angiopathy is a major complication of diabetes. Abnormally high blood glucose is a crucial risk factor for endothelial cell damage. Nuclear factor-κB (NF-κB) has been demonstrated as a mediated signaling in hyperglycemia or oxidative stress-triggered apoptosis of endothelial cells. Here we explored the efficacy of honokiol, a small molecular weight natural product, on NADPH oxidase-related oxidative stress-mediated NF-κB-regulated signaling and apoptosis in human umbilical vein endothelial cells (HUVECs) under hyperglycemic conditions. The methods of morphological Hoechst staining and annexin V/propidium iodide staining were used to detect apoptosis. Submicromolar concentrations of honokiol suppressed the increases of NADPH oxidase activity, Rac-1 phosphorylation, p22phox protein expression, and reactive oxygen species production in high glucose (HG)-stimulated HUVECs. The degradation of IκBα and increase of NF-κB activity were inhibited by honokiol in HG-treated HUVECs. Moreover, honokiol (0.125-1?μM) also suppressed HG-induced cyclooxygenase (COX)-2 upregulation and prostaglandin E2 production in HUVECs. Honokiol could reduce increased caspase-3 activity and the subsequent apoptosis and cell death triggered by HG. These results imply that inhibition of NADPH oxidase-related oxidative stress by honokiol suppresses the HG-induced NF-κB-regulated COX-2 upregulation, apoptosis, and cell death in HUVECs, which has the potential to be developed as a therapeutic agent to prevent hyperglycemia-induced endothelial damage. ? 2008 Elsevier B.V. All rights reserved. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/508560 | ISSN: | 0891-5849 | DOI: | 10.1016/j.freeradbiomed.2008.03.014 | SDG/關鍵字: | glucose; honokiol; protein p22; Rac1 protein; reduced nicotinamide adenine dinucleotide phosphate oxidase; apoptosis; article; controlled study; endothelium cell; enzyme activity; human; human cell; oxidative stress; priority journal; protein expression; protein phosphorylation; Apoptosis; Biphenyl Compounds; Cyclooxygenase 2; Endothelial Cells; Endothelium, Vascular; Enzyme Activation; Glucose; Humans; Lignans; NADPH Oxidase; NF-kappa B; Oxidative Stress; Phosphorylation; rac1 GTP-Binding Protein; Reactive Oxygen Species; Signal Transduction; Umbilical Veins |
顯示於: | 法醫學科所 |
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