ABSTRACT
Objective To explore the mechanism by which liraglutide modulated the differentiation of monocyte subsets in high glucose (HG) conditions.Methods Primary mouse splenocyte suspensions were cultured in HG conditions induced by IFN-γ in the presence or absence of liraglutide.The cells were harvested,co-incubated with antibodies,and analyzed on a BD FACS Calibur.Mononuclear cells (MNCs) were gated according to lower granularity and larger size by SSC and FSC.Monocytes (MCs) were defined as CD11b+MNC and divided into three subsets based on Ly6C expression:Ly6Clow,Ly6Cmid,and Ly6Chi.ROS production in Ly6C+ and Ly6C-MCs was detected by 2',7'-dichlorofluorescein-diacetate (DCFH-DA) staining and ROS-containing MCs were identified as DCF+ cells in both Ly6C+ and Ly6C-MCs.Results HG (15 mmol/L,25 mmol/L,35 mmol/L) dose-dependently increased Ly6Chi and Ly6Cmid MC differentiation and also enhanced the production of ROS in Ly6C+MCs.Liraglutide (100 U,200 U) dose-dependently inhibited HG-induced Ly6Chi and Ly6Cmid MC differentiation and also promoted the differentiation of Ly6Clow MCs.Moreover,liraglutide significantly inhibited HG-induced ROS production in Ly6C+ MCs.Conclusion Liraglutide treatment significantly inhibited inflammatory MC diferentiation induced by HG and also reduced ROS production in inflammatory MCs.