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

Molecules

Qian Li²  Yanli Qiu²  Min Mao¹  Jinying Lv²  Lixin Zhang¹  Shuzhen Li¹  Xia Li²  Xiaodong Zheng³ 

[1] Bio-pharmaceutical Key Laboratory of Harbin, Harbin Medical University, Harbin 150081, China; E-Mails:;Department of Pharmaceutical Analysis, College of Pharmacy, Harbin Medical University, Nangang District, Harbin 150081, China; E-Mails:;Department of Pathophysiology, Harbin Medical University-Daqing, Daqing 163319, China

关键词: rutin;    reactive oxygen species (ROS);    NADPH oxidase 4;    proliferation;    hypoxia;   

DOI  :  10.3390/molecules191119036

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.