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Publication : Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model.

First Author  Jia C Year  2014
Journal  PLoS One Volume  9
Issue  6 Pages  e99849
PubMed ID  24933211 Mgi Jnum  J:218860
Mgi Id  MGI:5618593 Doi  10.1371/journal.pone.0099849
Citation  Jia C, et al. (2014) Notoginsenoside R1 attenuates atherosclerotic lesions in ApoE deficient mouse model. PLoS One 9(6):e99849
abstractText  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-alpha and gamma-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.
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