Synthetic resveratrol aliphatic acid inhibits TLR2-mediated apoptosis and an involvement of Akt/GSK3β pathway

被引:26
作者
Chen, Lin [2 ,3 ]
Zhang, Yi [2 ]
Sun, Xiuli [4 ]
Li, Hui [2 ]
LeSage, Gene [2 ]
Javer, Avani [1 ]
Zhang, Xiumei [3 ]
Wei, Xinbing [3 ]
Jiang, Yulin [1 ]
Yin, Deling [2 ]
机构
[1] E Tennessee State Univ, Dept Chem, Johnson City, TN 37614 USA
[2] E Tennessee State Univ, Coll Med, Dept Internal Med, Johnson City, TN 37614 USA
[3] Shandong Univ, Sch Med, Dept Pharmacol, Jinan 250012, Peoples R China
[4] Peking Univ, Peoples Hosp, Dept Obstet & Gynecol, Beijing 100871, Peoples R China
基金
美国国家卫生研究院;
关键词
TLR2; Resveratrol; Apoptosis; Akt; GSK3; beta; GLYCOGEN-SYNTHASE KINASE-3; BREAST-CANCER CELLS; TOLL-LIKE RECEPTORS; ADAPTIVE IMMUNITY; INNATE IMMUNITY; STRESS; ACTIVATION; TLR2; REGULATIONS; RECOGNITION;
D O I
10.1016/j.bmc.2009.05.029
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
As resveratrol derivatives, resveratrol aliphatic acids were synthesized in our laboratory. Previously, we reported the improved pharmaceutical properties of the compounds compared to resveratrol, including better solubility in water and much tighter binding with human serum albumin. Here, we investigate the role of resveratrol aliphatic acids in Toll-like receptor 2 (TLR2)-mediated apoptosis. We showed that resveratrol aliphatic acid (R6A) significantly inhibits the expression of TLR2. In addition, overexpression of TLR2 in HEK293 cells caused a significant decrease in apoptosis after R6A treatment. Moreover, inhibition of TLR2 by R6A decreases serum deprivation-reduced the levels of phosphorylated Akt and phosphorylated glycogen synthase kinase 3 beta (GSK3 beta). Our study thus demonstrates that the resveratrol aliphatic acid inhibits cell apoptosis through TLR2 by the involvement of Akt/GSK3 beta pathway. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:4378 / 4382
页数:5
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