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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 3197829, 10 pages
https://doi.org/10.1155/2018/3197829
Research Article

Pu-erh Tea Ameliorates Atherosclerosis Associated with Promoting Macrophage Apoptosis by Reducing NF-κB Activation in ApoE Knockout Mice

1Department of Cardiovascular Medicine, First Affiliated Hospital of Xi’an Jiaotong University, 277 Yanta West Road, Xi’an, Shaanxi 710061, China
2Department of Rheumatology, First Affiliated Hospital of Xi’an Jiaotong University, 277 Yanta West Road, Xi’an, Shaanxi 710061, China
3Key Laboratory of Environment and Genes Related to Diseases, Xi’an Jiaotong University, Ministry of Education, Xi’an, Shaanxi 710061, China
4Key Laboratory of Molecular Cardiology, Xi’an Jiaotong University, Xi’an, Shaanxi 710061, China

Correspondence should be addressed to Zuyi Yuan; moc.361@415_wbs

Received 9 February 2018; Revised 6 May 2018; Accepted 20 May 2018; Published 23 August 2018

Academic Editor: Kota V. Ramana

Copyright © 2018 Yihui Xiao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

We explored whether pu-erh tea consumption ameliorates atherosclerosis and the possible mechanism for its effects in apolipoprotein E-deficient (ApoE−/−) mice. Our data showed that pu-erh tea consumption markedly reduced early fatty streak formation and the advanced fibrofatty plaque sizes. Additionally, the mean proportion of inflammatory macrophages in the plaque decreased, and the number of apoptotic macrophages increased significantly. NF-κB activity in peritoneal macrophages decreased by 75.6% compared to the controls, similar with the levels of IL-6, IL-12, and TNF-α expression. The tea extract increased the apoptosis of RAW264.7 cells by decreasing NF-κB activation and reducing the inflammatory cytokine expression. In conclusion, pu-erh tea ameliorates atherosclerosis progress by alleviating the chronic inflammatory state by reducing NF-κB activation and promoting macrophage apoptosis in atherosclerotic plaques.