摘要

In this study, the mechanisms by which pu-erh tea extract (PETE) attenuates nicotine-induced foam cell formation were investigated. Monocytes were purified from healthy individuals using commercial antibodies coated with magnetic beads. We found that the nicotine-induced (1-10 μM) expression of oxidized low-density lipoprotein receptors (ox-LDLRs) and α9-nAchRs in monocytes was significantly attenuated by 24 h of PETE (10 μg/mL; ∗, p < 0.05) cotreatment. Nicotine (1 μM for 24 h) significantly induced the expression of the surface adhesion molecule ICAM-1 and the monocyte integrin adhesion molecule (CD11b) by human umbilical vein endothelial cells (HUVECs) and triggered monocytes to differentiate into macrophages via interactions with the endothelium. After treatment with nicotine (0.1-10 μM for 24 h), the HUVECs released chemotactic factors (IL-8) to attract monocytes into the tunica intima of the artery, and the monocytes then transformed into foam cells. We demonstrated that PETE treatment (>1 μg/mL for 24 h; ∗, p < 0.05) significantly attenuates nicotine-induced (1 μM) monocyte migration toward HUVECs and foam cell formation. This study suggests that tea components effectively attenuate the initial step (foam cell formation) of nicotine-induced atherosclerosis in circulating monocytes.
原文英語
頁(從 - 到)3186-3195
頁數10
期刊Journal of Agricultural and Food Chemistry
64
發行號16
DOIs
出版狀態已發佈 - 四月 27 2016

指紋

foam cells
Foam Cells
nicotine
Tea
Nicotine
monocytes
tea
Foams
Monocytes
extracts
LDL Receptors
Human Umbilical Vein Endothelial Cells
low density lipoprotein
atherosclerosis
Atherosclerosis
receptors
antibodies
In Vitro Techniques
Antibodies

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Chemistry(all)

引用此文

Pu-erh Tea Extract Attenuates Nicotine-Induced Foam Cell Formation in Primary Cultured Monocytes : An in Vitro Mechanistic Study. / Tu, Shih Hsin; Chen, Ming Yao; Chen, Li Ching; Mao, Yi Ting; Ho, Chi Hou; Lee, Wen Jui; Lin, Yen-Kuang; Pan, Min Hsiung; Lo, Chih Yu; Chen, Chi Long; Yen, Yun; Whang-Peng, Jacqueline; Ho, Chi Tang; Wu, Chih Hsiung; Ho, Yuan Soon.

於: Journal of Agricultural and Food Chemistry, 卷 64, 編號 16, 27.04.2016, p. 3186-3195.

研究成果: 雜誌貢獻文章

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title = "Pu-erh Tea Extract Attenuates Nicotine-Induced Foam Cell Formation in Primary Cultured Monocytes: An in Vitro Mechanistic Study",
abstract = "In this study, the mechanisms by which pu-erh tea extract (PETE) attenuates nicotine-induced foam cell formation were investigated. Monocytes were purified from healthy individuals using commercial antibodies coated with magnetic beads. We found that the nicotine-induced (1-10 μM) expression of oxidized low-density lipoprotein receptors (ox-LDLRs) and α9-nAchRs in monocytes was significantly attenuated by 24 h of PETE (10 μg/mL; ∗, p <0.05) cotreatment. Nicotine (1 μM for 24 h) significantly induced the expression of the surface adhesion molecule ICAM-1 and the monocyte integrin adhesion molecule (CD11b) by human umbilical vein endothelial cells (HUVECs) and triggered monocytes to differentiate into macrophages via interactions with the endothelium. After treatment with nicotine (0.1-10 μM for 24 h), the HUVECs released chemotactic factors (IL-8) to attract monocytes into the tunica intima of the artery, and the monocytes then transformed into foam cells. We demonstrated that PETE treatment (>1 μg/mL for 24 h; ∗, p <0.05) significantly attenuates nicotine-induced (1 μM) monocyte migration toward HUVECs and foam cell formation. This study suggests that tea components effectively attenuate the initial step (foam cell formation) of nicotine-induced atherosclerosis in circulating monocytes.",
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author = "Tu, {Shih Hsin} and Chen, {Ming Yao} and Chen, {Li Ching} and Mao, {Yi Ting} and Ho, {Chi Hou} and Lee, {Wen Jui} and Yen-Kuang Lin and Pan, {Min Hsiung} and Lo, {Chih Yu} and Chen, {Chi Long} and Yun Yen and Jacqueline Whang-Peng and Ho, {Chi Tang} and Wu, {Chih Hsiung} and Ho, {Yuan Soon}",
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T2 - An in Vitro Mechanistic Study

AU - Tu, Shih Hsin

AU - Chen, Ming Yao

AU - Chen, Li Ching

AU - Mao, Yi Ting

AU - Ho, Chi Hou

AU - Lee, Wen Jui

AU - Lin, Yen-Kuang

AU - Pan, Min Hsiung

AU - Lo, Chih Yu

AU - Chen, Chi Long

AU - Yen, Yun

AU - Whang-Peng, Jacqueline

AU - Ho, Chi Tang

AU - Wu, Chih Hsiung

AU - Ho, Yuan Soon

PY - 2016/4/27

Y1 - 2016/4/27

N2 - In this study, the mechanisms by which pu-erh tea extract (PETE) attenuates nicotine-induced foam cell formation were investigated. Monocytes were purified from healthy individuals using commercial antibodies coated with magnetic beads. We found that the nicotine-induced (1-10 μM) expression of oxidized low-density lipoprotein receptors (ox-LDLRs) and α9-nAchRs in monocytes was significantly attenuated by 24 h of PETE (10 μg/mL; ∗, p <0.05) cotreatment. Nicotine (1 μM for 24 h) significantly induced the expression of the surface adhesion molecule ICAM-1 and the monocyte integrin adhesion molecule (CD11b) by human umbilical vein endothelial cells (HUVECs) and triggered monocytes to differentiate into macrophages via interactions with the endothelium. After treatment with nicotine (0.1-10 μM for 24 h), the HUVECs released chemotactic factors (IL-8) to attract monocytes into the tunica intima of the artery, and the monocytes then transformed into foam cells. We demonstrated that PETE treatment (>1 μg/mL for 24 h; ∗, p <0.05) significantly attenuates nicotine-induced (1 μM) monocyte migration toward HUVECs and foam cell formation. This study suggests that tea components effectively attenuate the initial step (foam cell formation) of nicotine-induced atherosclerosis in circulating monocytes.

AB - In this study, the mechanisms by which pu-erh tea extract (PETE) attenuates nicotine-induced foam cell formation were investigated. Monocytes were purified from healthy individuals using commercial antibodies coated with magnetic beads. We found that the nicotine-induced (1-10 μM) expression of oxidized low-density lipoprotein receptors (ox-LDLRs) and α9-nAchRs in monocytes was significantly attenuated by 24 h of PETE (10 μg/mL; ∗, p <0.05) cotreatment. Nicotine (1 μM for 24 h) significantly induced the expression of the surface adhesion molecule ICAM-1 and the monocyte integrin adhesion molecule (CD11b) by human umbilical vein endothelial cells (HUVECs) and triggered monocytes to differentiate into macrophages via interactions with the endothelium. After treatment with nicotine (0.1-10 μM for 24 h), the HUVECs released chemotactic factors (IL-8) to attract monocytes into the tunica intima of the artery, and the monocytes then transformed into foam cells. We demonstrated that PETE treatment (>1 μg/mL for 24 h; ∗, p <0.05) significantly attenuates nicotine-induced (1 μM) monocyte migration toward HUVECs and foam cell formation. This study suggests that tea components effectively attenuate the initial step (foam cell formation) of nicotine-induced atherosclerosis in circulating monocytes.

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