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Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline

BACKGROUND: Cigarette smoke (CS) exposure impaired plasma lipid profiles by modification of apolipoproteins. Hydrogen (H(2)) has been proved effective on reducing oxidative stress or improving HDL functionalities in animal models or metabolic syndrome volunteers. This study was undertaken to explore...

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Autores principales: Zong, Chuanlong, Song, Guohua, Yao, Shutong, Guo, Shoudong, Yu, Yang, Yang, Nana, Guo, Zheng, Qin, Shucun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668613/
https://www.ncbi.nlm.nih.gov/pubmed/26634341
http://dx.doi.org/10.1186/s12944-015-0160-9
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author Zong, Chuanlong
Song, Guohua
Yao, Shutong
Guo, Shoudong
Yu, Yang
Yang, Nana
Guo, Zheng
Qin, Shucun
author_facet Zong, Chuanlong
Song, Guohua
Yao, Shutong
Guo, Shoudong
Yu, Yang
Yang, Nana
Guo, Zheng
Qin, Shucun
author_sort Zong, Chuanlong
collection PubMed
description BACKGROUND: Cigarette smoke (CS) exposure impaired plasma lipid profiles by modification of apolipoproteins. Hydrogen (H(2)) has been proved effective on reducing oxidative stress or improving HDL functionalities in animal models or metabolic syndrome volunteers. This study was undertaken to explore the effects of CS exposure on reverse cholesterol transport (RCT) and the antioxidative effects of H(2) treatment against CS exposure in mice transgenic for human cholesteryl ester transfer protein (CETP). METHODS: [(3)H]-cholesterol-laden macrophages were injected intraperitoneally into mice, and the samples of blood, bile, liver, and feces were collected for radioactivity determination to evaluate RCT. [(3)H]-cholesterol-laden macrophages were incubated with HDL isolated from different groups of mice, and the samples of cell medium supernatants were collected for evaluating the HDL functionality to elicit cholesterol efflux. RESULTS: CS exposure significantly decreased plasma HDL cholesterol level (HDL-C) by 22 % and increased LDL cholesterol level (LDL-C) by 21 % compared with the control group (p < 0.05, p < 0.01), while H(2) treatment significantly improved the CS-impaired levels of TC, LDL-C and HDL-C by 10, 27 and 31 %, respectively, compared with the CS group (p < 0.05, p < 0.01 and p < 0.05). Besides, CS exposure significantly decreased [(3)H] tracer concentrations in liver, bile and feces by 17, 35 and 48 %, respectively, compared with the control group (p < 0.05 for liver and feces), while H(2) treatment significantly improved them by 21, 72 % and 89 %, respectively, compared with the CS group (all p < 0.05). Furthermore, CS exposure significantly decreased the HDL functionality to elicit cholesterol efflux by 26 % (p < 0.05), while H(2) treatment also improved it by 32 % (p < 0.05). We did not find any significant alterations in protein expressions of RCT involved genes. CONCLUSIONS: These findings provided direct evidence supporting the notion that CS exposure in vivo impairs plasma lipid profiles, HDL functionalities and macrophage-to-feces RCT pathway in CETP transgenic mice, all of which can be minimized by treatment of H(2)-saturated saline.
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spelling pubmed-46686132015-12-04 Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline Zong, Chuanlong Song, Guohua Yao, Shutong Guo, Shoudong Yu, Yang Yang, Nana Guo, Zheng Qin, Shucun Lipids Health Dis Research BACKGROUND: Cigarette smoke (CS) exposure impaired plasma lipid profiles by modification of apolipoproteins. Hydrogen (H(2)) has been proved effective on reducing oxidative stress or improving HDL functionalities in animal models or metabolic syndrome volunteers. This study was undertaken to explore the effects of CS exposure on reverse cholesterol transport (RCT) and the antioxidative effects of H(2) treatment against CS exposure in mice transgenic for human cholesteryl ester transfer protein (CETP). METHODS: [(3)H]-cholesterol-laden macrophages were injected intraperitoneally into mice, and the samples of blood, bile, liver, and feces were collected for radioactivity determination to evaluate RCT. [(3)H]-cholesterol-laden macrophages were incubated with HDL isolated from different groups of mice, and the samples of cell medium supernatants were collected for evaluating the HDL functionality to elicit cholesterol efflux. RESULTS: CS exposure significantly decreased plasma HDL cholesterol level (HDL-C) by 22 % and increased LDL cholesterol level (LDL-C) by 21 % compared with the control group (p < 0.05, p < 0.01), while H(2) treatment significantly improved the CS-impaired levels of TC, LDL-C and HDL-C by 10, 27 and 31 %, respectively, compared with the CS group (p < 0.05, p < 0.01 and p < 0.05). Besides, CS exposure significantly decreased [(3)H] tracer concentrations in liver, bile and feces by 17, 35 and 48 %, respectively, compared with the control group (p < 0.05 for liver and feces), while H(2) treatment significantly improved them by 21, 72 % and 89 %, respectively, compared with the CS group (all p < 0.05). Furthermore, CS exposure significantly decreased the HDL functionality to elicit cholesterol efflux by 26 % (p < 0.05), while H(2) treatment also improved it by 32 % (p < 0.05). We did not find any significant alterations in protein expressions of RCT involved genes. CONCLUSIONS: These findings provided direct evidence supporting the notion that CS exposure in vivo impairs plasma lipid profiles, HDL functionalities and macrophage-to-feces RCT pathway in CETP transgenic mice, all of which can be minimized by treatment of H(2)-saturated saline. BioMed Central 2015-12-03 /pmc/articles/PMC4668613/ /pubmed/26634341 http://dx.doi.org/10.1186/s12944-015-0160-9 Text en © Zong et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Zong, Chuanlong
Song, Guohua
Yao, Shutong
Guo, Shoudong
Yu, Yang
Yang, Nana
Guo, Zheng
Qin, Shucun
Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline
title Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline
title_full Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline
title_fullStr Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline
title_full_unstemmed Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline
title_short Cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline
title_sort cigarette smoke exposure impairs reverse cholesterol transport which can be minimized by treatment of hydrogen-saturated saline
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668613/
https://www.ncbi.nlm.nih.gov/pubmed/26634341
http://dx.doi.org/10.1186/s12944-015-0160-9
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