Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.

AIMS: Atherosclerosis is the primary cause of cardiovascular diseases and stroke. The current study evaluated the interventional effects of a naturally occurring compound Notoginsenoside R1 (NR1) on atherosclerosis in ApoE-/- mice. METHODS AND RESULTS: The atherosclerotic lesion was significantly al...

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Main Authors: Chenglin Jia, Minqi Xiong, Peiwei Wang, Jingang Cui, Xiaoye Du, Qinbo Yang, Wenjian Wang, Yu Chen, Teng Zhang
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4059705?pdf=render
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spelling doaj-b8ba75710a914a2680e46af22f7067962020-11-25T00:47:27ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0196e9984910.1371/journal.pone.0099849Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.Chenglin JiaMinqi XiongPeiwei WangJingang CuiXiaoye DuQinbo YangWenjian WangYu ChenTeng ZhangAIMS: Atherosclerosis is the primary cause of cardiovascular diseases and stroke. The current study evaluated the interventional effects of a naturally occurring compound Notoginsenoside R1 (NR1) on atherosclerosis in ApoE-/- mice. METHODS AND RESULTS: The atherosclerotic lesion was significantly alleviated by NR1 treatment and this attenuation was marked by reduction in lipid deposition, fibrosis and oxidative stress. Increased serum levels of GSH and SOD and decreased level of MDH were observed in NR1-treated ApoE-/- mice. NR1 treatment also significantly decreased the levels of CHO, TG, ox-LDL and increased the level of HDL. Additionally, the levels of inflammatory cytokines including IL-2, IL-6, TNF-α and γ-IFN were markedly reduced in NR1-treated ApoE-/- mice. Furthermore, significantly increased aortic expression of miR-26a, miR-21, miR-126a, miR-132, miR-146 and miR-155 and decreased expression of miR-20a and miR-92a were observed in the vehicle-treated ApoE-/- mice. While NR1 treatment led to a significant reduction in the expression of miR-21, miR-26a, miR-126 and increased expression of miR-20a. CONCLUSION: Collectively, our results demonstrated for the first time the anti-atherosclerotic effects of NR1, which could be in part mediated through its multiple targeting effects on inflammation, oxidative stress, lipid metabolism and microRNA expression. These results therefore justify further evaluation of NR1 as a therapeutic agent treating atherosclerosis.http://europepmc.org/articles/PMC4059705?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Chenglin Jia
Minqi Xiong
Peiwei Wang
Jingang Cui
Xiaoye Du
Qinbo Yang
Wenjian Wang
Yu Chen
Teng Zhang
spellingShingle Chenglin Jia
Minqi Xiong
Peiwei Wang
Jingang Cui
Xiaoye Du
Qinbo Yang
Wenjian Wang
Yu Chen
Teng Zhang
Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
PLoS ONE
author_facet Chenglin Jia
Minqi Xiong
Peiwei Wang
Jingang Cui
Xiaoye Du
Qinbo Yang
Wenjian Wang
Yu Chen
Teng Zhang
author_sort Chenglin Jia
title Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
title_short Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
title_full Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
title_fullStr Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
title_full_unstemmed Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.
title_sort notoginsenoside r1 attenuates atherosclerotic lesions in apoe deficient mouse model.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2014-01-01
description AIMS: Atherosclerosis is the primary cause of cardiovascular diseases and stroke. The current study evaluated the interventional effects of a naturally occurring compound Notoginsenoside R1 (NR1) on atherosclerosis in ApoE-/- mice. METHODS AND RESULTS: The atherosclerotic lesion was significantly alleviated by NR1 treatment and this attenuation was marked by reduction in lipid deposition, fibrosis and oxidative stress. Increased serum levels of GSH and SOD and decreased level of MDH were observed in NR1-treated ApoE-/- mice. NR1 treatment also significantly decreased the levels of CHO, TG, ox-LDL and increased the level of HDL. Additionally, the levels of inflammatory cytokines including IL-2, IL-6, TNF-α and γ-IFN were markedly reduced in NR1-treated ApoE-/- mice. Furthermore, significantly increased aortic expression of miR-26a, miR-21, miR-126a, miR-132, miR-146 and miR-155 and decreased expression of miR-20a and miR-92a were observed in the vehicle-treated ApoE-/- mice. While NR1 treatment led to a significant reduction in the expression of miR-21, miR-26a, miR-126 and increased expression of miR-20a. CONCLUSION: Collectively, our results demonstrated for the first time the anti-atherosclerotic effects of NR1, which could be in part mediated through its multiple targeting effects on inflammation, oxidative stress, lipid metabolism and microRNA expression. These results therefore justify further evaluation of NR1 as a therapeutic agent treating atherosclerosis.
url http://europepmc.org/articles/PMC4059705?pdf=render
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