Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model

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. The atherosclerotic lesion was significantly alleviated by NR1 treatment a...

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Published inPloS one Vol. 9; no. 6; p. e99849
Main Authors Jia, Chenglin, Xiong, Minqi, Wang, Peiwei, Cui, Jingang, Du, Xiaoye, Yang, Qinbo, Wang, Wenjian, Chen, Yu, Zhang, Teng
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 16.06.2014
Public Library of Science (PLoS)
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Summary: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. 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. 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.
Bibliography:Conceived and designed the experiments: CJ MX YC TZ. Performed the experiments: PW JC QY XD. Analyzed the data: CJ MX WW YC TZ. Contributed to the writing of the manuscript: YC TZ.
Competing Interests: The authors have declared that no competing interests exist.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0099849