Journal
MOLECULES
Volume 19, Issue 11, Pages 19036-19049Publisher
MDPI AG
DOI: 10.3390/molecules191119036
Keywords
rutin; reactive oxygen species (ROS); NADPH oxidase 4; proliferation; hypoxia
Funding
- National Natural Science Foundation of China [31100835]
- National Foundation for Post-doctoral Scholars [2013M531066]
- Heilongjiang Province Foundation for Post-doctoral Scholars [LBH-Z11059]
- Heilongjiang Province Education Department [12511316]
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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-1 alpha (HIF-1 alpha). 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.
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