Salusin-α attenuates inflammatory responses in vascular endothelial cells
- Authors: Esfahani M.1, Saidijam M.2, Goodarzi M.T.2,3, Movahedian A.1, Najafi R.2
-
Affiliations:
- Isfahan University of Medical Sciences, School of Pharmacy and Pharmaceutical Sciences and Isfahan Pharmaceutical Sciences Research Center
- Research Center for Molecular Medicine
- Hamadan University of Medical Sciences, School of Medicine
- Issue: Vol 82, No 11 (2017)
- Pages: 1314-1323
- Section: Article
- URL: https://journals.rcsi.science/0006-2979/article/view/151508
- DOI: https://doi.org/10.1134/S0006297917110098
- ID: 151508
Cite item
Abstract
Atherosclerosis accounts for numerous cardiovascular diseases, and cytokines have a critical role in acceleration or suppression of disease. Salusin-α presents a new class of bioactive peptides that can have anti-atherogenic properties. Therefore, the effects of salusin-α on the expression of some pro- and anti-inflammatory cytokines and on TNF-α-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs) were examined. The involvement of the NF-κB pathway in effects of salusin-α in HUVECs was checked using Bay 11-7082 as an NF-κB inhibitor. The mRNA expression of pro-inflammatory cytokines including IL-6, IL-8, and IL-18 and anti-inflammatory cytokine IL-1Ra was assessed by real-time PCR. The protein levels of cytokines were measured by the ELISA method. Salusin-α suppressed both mRNA and protein expression of pro-inflammatory cytokines and induced mRNA and protein expression of IL-1Ra in HUVECs. Salusin-α suppressed TNF-α-induced inflammatory responses in HUVECs. The down-regulatory or up-regulatory effects of salusin-α on expression of cytokines could not be influenced by Bay 11-7082 pretreatment. Our findings indicate anti-inflammatory effects of salusin-α and suggest a novel peptide-based therapeutic strategy for atherosclerosis.
Keywords
About the authors
Maryam Esfahani
Isfahan University of Medical Sciences, School of Pharmacy and Pharmaceutical Sciences and Isfahan Pharmaceutical Sciences Research Center
Email: najafi2535@gmail.com
Iran, Islamic Republic of, Isfahan
Masoud Saidijam
Research Center for Molecular Medicine
Email: najafi2535@gmail.com
Iran, Islamic Republic of, Hamadan
Mohammad Taghi Goodarzi
Research Center for Molecular Medicine; Hamadan University of Medical Sciences, School of Medicine
Email: najafi2535@gmail.com
Iran, Islamic Republic of, Hamadan; Hamadan
Ahmad Movahedian
Isfahan University of Medical Sciences, School of Pharmacy and Pharmaceutical Sciences and Isfahan Pharmaceutical Sciences Research Center
Author for correspondence.
Email: Movahedian@pharm.mui.ac.ir
Iran, Islamic Republic of, Isfahan
Rezvan Najafi
Research Center for Molecular Medicine
Author for correspondence.
Email: najafi2535@gmail.com
Iran, Islamic Republic of, Hamadan