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Dihydroartemisinin ameliorates balloon injury-induced neointimal formation in rats.

Authors :
He Y
Sun B
Chen G
Huang R
Source :
Journal of cellular physiology [J Cell Physiol] 2019 Jul; Vol. 234 (7), pp. 11545-11554. Date of Electronic Publication: 2018 Dec 03.
Publication Year :
2019

Abstract

Objectives: This study aims to evaluate the effects of dihydroartemisinin (DHA) on the balloon injury-induced neointimal formation in rats and to investigate the underlying mechanism.<br />Methods: The balloon-induced carotid artery injury model was established in male Sprague-Dawley rats, immediately after which the DHA solution was injected into the tail vein of rats. In in vitro assays, primary rat vascular smooth muscle cells (VSMCs) were pretreated with DHA and then coincubated with LPS.<br />Results: DHA ameliorated the induced neointimal formation and fibrosis but enhanced apoptosis in rat carotid artery after balloon injury. Furthermore, DHA suppressed migration and enhanced apoptosis of the lipopolysaccharide (LPS)-treated primary VSMCs in vitro. Moreover, in both the balloon injury-induced rat sera and the LPS-treated VSMCs, DHA significantly inhibited proinflammatory cytokines, including interleukin-1β, tumor necrosis factor-ɑ, and matrix metalloproteinase-1. Importantly, DHA significantly decreased the balloon injury-increased expression of nuclear factor kappa B (NF-κB) subunit NF-κB p65 expression, and increased the balloon injury-reduced expression of inhibitor of NF-κB-alpha, indicating the inhibition of the IκB/NF-κB pathway.<br />Conclusion: DHA significantly inhibited neointimal formation in balloon-induced rat carotid artery injury and the mechanism may be related to the inhibition of IκB/NF-κB signaling, which alleviates the inflammatory response.<br /> (© 2018 Wiley Periodicals, Inc.)

Details

Language :
English
ISSN :
1097-4652
Volume :
234
Issue :
7
Database :
MEDLINE
Journal :
Journal of cellular physiology
Publication Type :
Academic Journal
Accession number :
30511399
Full Text :
https://doi.org/10.1002/jcp.27809