Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells

  • Authors:
    • Jin Jiang
    • Zhong-Cheng Mo
    • Kai Yin
    • Guo-Jun Zhao
    • Yun-Cheng Lv
    • Xin-Ping Ouyang
    • Zhi-Sheng Jiang
    • Yuchang Fu
    • Chao-Ke Tang
  • View Affiliations

  • Published online on: February 21, 2012     https://doi.org/10.3892/ijmm.2012.924
  • Pages: 946-956
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The ATP-binding membrane cassette transporter A1 (ABCA1) plays a protective role in the development of atherosclerosis for the reverse cholesterol transport process. Epigallocatechin-3-gallate (EGCG), which exists abundantly in green tea, exerts an anti-atherosclerotic effect via anti-inflammatory and metabolic regulation activities. Many genes and proteins related to lipid metabolism are involved in the lowering cholesterol effects of EGCG. However, effects of EGCG on ABCA1 have rarely been described. In the study presented here, we found that exposure of macrophage foam cells to TNF-α results in a downregulation of ABCA1 and a decrease in cholesterol efflux to apoA1, which is attenuated by pretreatment with EGCG. Moreover, rather than activating the Liver X receptor (LXR) pathway, inhibition of the TNF-α-induced nuclear factor-κB (NF-κB) activity is detected with EGCG treatment in cells. In order to inhibit the NF-κB activity, EGCG can promote the dissociation of the nuclear factor E2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) complex; when the released Nrf2 translocates to the nucleus and activates the transcription of genes containing an ARE element inhibition of NF-κB occurs and Keap1 is separated from the complex to directly interact with IKKβ and thus represses NF-κB function. These results provide novel insight into the anti-inflammatory effects of EGCG, as well as the identification of a novel potential therapeutic role for the prevention of atherosclerosis.

Related Articles

Journal Cover

May 2012
Volume 29 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Jiang J, Mo Z, Yin K, Zhao G, Lv Y, Ouyang X, Jiang Z, Fu Y and Tang C: Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells. Int J Mol Med 29: 946-956, 2012.
APA
Jiang, J., Mo, Z., Yin, K., Zhao, G., Lv , Y., Ouyang, X. ... Tang, C. (2012). Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells. International Journal of Molecular Medicine, 29, 946-956. https://doi.org/10.3892/ijmm.2012.924
MLA
Jiang, J., Mo, Z., Yin, K., Zhao, G., Lv , Y., Ouyang, X., Jiang, Z., Fu, Y., Tang, C."Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells". International Journal of Molecular Medicine 29.5 (2012): 946-956.
Chicago
Jiang, J., Mo, Z., Yin, K., Zhao, G., Lv , Y., Ouyang, X., Jiang, Z., Fu, Y., Tang, C."Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells". International Journal of Molecular Medicine 29, no. 5 (2012): 946-956. https://doi.org/10.3892/ijmm.2012.924