Salusin-α Attenuates Inflammatory Responses in Vascular Endothelial Cells

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Maryam Esfahani¹, Masoud Saidijam², Mohammad Taghi Goodarzi^2,3, Ahmad Movahedian^1*, and Rezvan Najafi^2*

¹Isfahan University of Medical Sciences, School of Pharmacy and Pharmaceutical Sciences and Isfahan Pharmaceutical Sciences Research Center, Department of Clinical Biochemistry, Isfahan, Iran; E-mail: Movahedian@pharm.mui.ac.ir

²Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, Iran; E-mail: najafi2535@gmail.com

³Hamadan University of Medical Sciences, School of Medicine, Department of Clinical Biochemistry, Hamadan, Iran

^* To whom correspondence should be addressed.

Received April 3, 2017; Revision received August 7, 2017

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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.

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KEY WORDS: atherosclerosis, salusin-α, inflammation, endothelial cells, cytokines

DOI: 10.1134/S0006297917110098

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