Next Article in Journal
Synthesis and Biological Evaluation of New Pleuromutilin Derivatives as Antibacterial Agents
Previous Article in Journal
Design, Synthesis, and Biological Evaluation of Artemisinin-Indoloquinoline Hybrids as Potent Antiproliferative Agents
Article Menu

Export Article

Open AccessArticle
Molecules 2014, 19(11), 19036-19049; doi:10.3390/molecules191119036

Antioxidant Mechanism of Rutin on Hypoxia-Induced Pulmonary Arterial Cell Proliferation

1,†
,
1,†
,
2,3
,
1
,
2,3
,
2,3
,
1
and
3,*
1
Department of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Nangang District, Harbin 150081, China
2
Bio-pharmaceutical Key Laboratory of Harbin, Harbin Medical University, Harbin 150081, China
3
Department of Pathophysiology, Harbin Medical University-Daqing, Daqing 163319, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 26 August 2014 / Revised: 28 September 2014 / Accepted: 9 October 2014 / Published: 18 November 2014
(This article belongs to the Section Natural Products)
View Full-Text   |   Download PDF [2948 KB, uploaded 18 November 2014]   |  

Abstract

Reactive oxygen species (ROS) are involved in the pathologic process of pulmonary arterial hypertension as either mediators or inducers. Rutin is a type of flavonoid which exhibits significant scavenging properties on oxygen radicals both in vitro and in vivo. In this study, we proposed that rutin attenuated hypoxia-induced pulmonary artery smooth muscle cell (PASMC) proliferation by scavenging ROS. Immunofluorescence data showed that rutin decreased the production of ROS, which was mainly generated through mitochondria and NADPH oxidase 4 (Nox4) in pulmonary artery endothelial cells (PAECs). Western blot results provided further evidence on rutin increasing expression of Nox4 and hypoxia-inducible factor-1α (HIF-1α). Moreover, cell cycle analysis by flow cytometry indicated that proliferation of PASMCs triggered by hypoxia was also repressed by rutin. However, N-acetyl-L-cysteine (NAC), a scavenger of ROS, abolished or diminished the capability of rutin in repressing hypoxia-induced cell proliferation. These data suggest that rutin shows a potential benefit against the development of hypoxic pulmonary arterial hypertension by inhibiting ROS, subsequently preventing hypoxia-induced PASMC proliferation. View Full-Text
Keywords: rutin; reactive oxygen species (ROS); NADPH oxidase 4; proliferation; hypoxia rutin; reactive oxygen species (ROS); NADPH oxidase 4; proliferation; hypoxia
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Li, Q.; Qiu, Y.; Mao, M.; Lv, J.; Zhang, L.; Li, S.; Li, X.; Zheng, X. Antioxidant Mechanism of Rutin on Hypoxia-Induced Pulmonary Arterial Cell Proliferation. Molecules 2014, 19, 19036-19049.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]

Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top