Abstract:Aim To investigate the effect of irisin on endothelial inflammation and atherosclerosis (As) in mice. Methods ApoE－/－ mice were randomly divided into control group, As model group, and irisin group (treated with irisin based on the As model), with 10 mice in each group. The carotid tissues were stained using pathological techniques and immunofluorescence. Human aortic endothelial cells (HAEC) were cultured in vitro, treated with irisin, and stimulated with cholesterol crystal (CC). The protein levels of vascular cell adhesion molecule-1(VCAM-1) and intercellular cell adhesion molecule-1(ICAM-1) were then detected by Western blot. The expression of inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and chemokine (C-C motif) ligand 2 (CCL2) were detected by RT-qPCR. The adhesion of monocytes was assessed using cell adhesion assay. Results The carotid plaque area in the mice of As model group was significantly increased compared with that in control group (P＜0.05). In contrast, the plaque area was reduced in the irisin group compared with the As model group (P＜0.05). Compared with the control group, the expression of VCAM-1, the number of CD68＋ macrophages, and the deposition of CC were increased in the carotid arteries of the As model group (P＜0.05), while irisin could reduce the expression of VCAM-1, the number of CD68＋ macrophages, and the deposition of CC (P＜0.05). At the in vitro level, the expression of VCAM-1 and ICAM-1, as well as the adhesion of monocytes in CC-stimulated HAEC, were increased (P＜0.05). However, irisin could inhibit the increased expression of VCAM-1 and ICAM-1 (P＜0.05), as well as the adhesion of monocytes induced by CC (P＜0.05). The mRNA levels of IL-1β, IL-6 and CCL2 in HAEC of CC stimulated group were increased (P＜0.05), while irisin could inhibit the mRNA expressions of IL-1β, IL-6 and CCL2 induced by CC (P＜0.05). Conclusion Irisin can inhibit vascular inflammation, thereby reducing the occurrence and progression of atherosclerosis.
