Maryam Esfahani - Isfahan Pharmaceutical Sciences Research Center AND Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
Masoud Saidijam - Professor, Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
Rezvan Najafi - Assistant Professor, Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
Mohammad Taghi Goodarzi - Professor, Research Center for Molecular Medicine AND Department of Clinical Biochemistry, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
Ahmad Movahedian - Professor, Isfahan Pharmaceutical Sciences Research Center AND Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran

BACKGROUND: Atherosclerosis is one of the predominant causes of cardiovascular disease (CVD). Several studies indicated the significant pathophysiological role of salusin-β in atherosclerosis. Cytokines are involved in all stages of atherosclerosis. Therefore, we aimed to assess the effect of salusin-β on interleukin ۶ (IL-۶), interleukin ۸ (IL-۸), interleukin ۱۸ (IL-۱۸) (as inflammatory cytokines) and interleukin ۱Ra (IL-۱Ra) (as anti-inflammatory cytokines) levels in human umbilical vein endothelial cells (HUVECs).METHODS: The HUVECs were cultured in HUVEC completed medium and treated with different doses of salusin-β for ۶ and ۱۲ hours. For the investigation of nuclear factor ƙβ (NF-ƙβ) signaling pathway involvement, cells were treated in the presence or absence of Bay ۱۱-۷۰۸۲ (as NF-ƙβ inhibitor). The mRNA expression and protein level of cytokines were measured by a real-time polymerase chain reaction (PCR) system and enzyme-linked immunosorbent assay (ELISA) method, respectively.RESULTS: Salusin-β increased mRNA expression and protein level of IL-۶, IL-۸ and IL-۱۸. This protein decreased mRNA and protein level of IL-۱Ra in HUVECs. NF-ƙβ signaling pathway was involved in the up-regulatory effect of salusin-β on mRNA expression of pro-inflammatory cytokines. The down-regulatory effect of salusin-β on IL-۱Ra expression could not be influenced by Bay ۱۱-۷۰۸۲ pre-treatment.CONCLUSION: It seems that salusin-β may participate in a cascade pathway in vascular inflammation. Our findings suggested that salusin-β has potential use as a therapeutic target for atherosclerosis.

Atherosclerosis, Cardiovascular Diseases, Cytokines, Endothelial Cells, Inflammation, Salusin-Beta