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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.
Chiang, C.K.
Tsai, K.S.
Ho, F.M.
Weng, T.I.
Wu, H.Y.
Liu, S.H.
關鍵字: honokiol
human umbilical vein endothelial cells
reactive oxygen species
NF-kappa B
ischemia-reperfusion injury
oxygen species production
cyclooxygenase-2 expression
p65 phosphorylation
mesangial cells
alpha kinase
diabetic rat
期刊/報告no:: Free Radical Biology and Medicine, Volume 44, Issue 12, Page(s) 2043-2050.
摘要: Angiopathy is a major complication of diabetes. Abnormally high blood glucose is a crucial risk factor for endothelial cell damage. Nuclear factor-kappa B (NF-kappa B) 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-kappa B-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, p22(phox) protein expression, and reactive oxygen species production in high glucose (HG)-stimulated HUVECs. The degradation of I kappa B alpha and increase of NF-K beta activity were inhibited by honokiol in HG-treated HUVECs. Moreover, honokiol (0.125-1 mu M) also suppressed HG-induced cyclooxygenase (COX)-2 upregulation and prostaglandin E(2) 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-kappa B-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. (C) 2008 Elsevier Inc. All rights reserved.
ISSN: 0891-5849
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