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Modafinil improves monocrotaline-induced pulmonary hypertension rat model

Title
Modafinil improves monocrotaline-induced pulmonary hypertension rat model
Authors
Lee, HyeryonKim, Kwan ChangCho, Min-SunSuh, Suk-hyoHong, Young Mi
Ewha Authors
홍영미서석효조민선김관창
SCOPUS Author ID
홍영미scopus; 서석효scopus; 조민선scopus; 김관창scopus
Issue Date
2016
Journal Title
PEDIATRIC RESEARCH
ISSN
0031-3998JCR Link1530-0447JCR Link
Citation
vol. 80, no. 1, pp. 119 - 127
Publisher
NATURE PUBLISHING GROUP
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
BACKGROUND: Pulmonary arterial hypertension (PAH) progressively leads to increases in pulmonary vasoconstriction. Modafinil plays a role in vasorelaxation and blocking KCa3.1 channel with a result of elevating intracellular cyclic adenosine monophosphate (cAMP) levels. The purpose of this study is to evaluate the effects on modafinil in monocrotaline (MCT)-induced PAH rat. METHODS: The rats were separated into three groups: the control group, the monocrotaline (M) group (MCT 60 mg/kg), and the modafinil (MD) group (MCT 60 mg/kg + modafinil). RESULTS: Reduced right ventricular pressure (RVP) was observed in the MD group. Right ventricular hypertrophy was improved in the MD group. Reduced number of intra-acinar pulmonary arteries and medial wall thickness were noted in the MD group. After the administration of modafinil, protein expressions of endothelin-1 (ET-1), endothelin receptor A (ERA) and KCa3.1 channel were significantly reduced. Modafinil suppressed pulmonary artery smooth muscle cell (PASMC) proliferation via cAMP and KCa3.1 channel. Additionally, we confirmed protein expressions such as Bcl-2-associated X, vascular endothelial growth factor, tumor necrosis factor-alpha, and interleukin-6 were reduced in the MD group. CONCLUSION: Modafinil improved PAH by vasorelaxation and a decrease in medial thickening via ET-1, ERA, and KCa3.1 down regulation. This is a meaningful study of a modafinil in PAH model.
DOI
10.1038/pr.2016.38
Appears in Collections:
의과대학 > 의학과 > Journal papers
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