Fig. 6

LY333531 inhibited the immune maturation of DCs and alleviated atherosclerosis in diabetic ApoE^−/− mice. The expression of the co-stimulatory molecules, CD83 and CD86, in splenic DCs was inhibited in the LY333531 group (a). The qPCR results also indicated that the expressions of TNFα, IL12b, IL6, CCL4, CCR7, and CXCR4 were inhibited in DCs, while the expression of IL10 was increased (b, c). In the LY333531 group, not only were the aortic adhesion molecules, ICAM1 and VCAM1, inhibited (d), but inflammatory markers such as TNFα, IFNγ, and CRP also were inhibited in peripheral blood (e, f). Systemic administration of LY333531 delayed the formation of aortic root plaques in mice with diabetic atherosclerosis when compared with the control group (g). Masson staining revealed that the collagen fiber composition in the plaques increased (h). Staining of cells in the plaque indicated that the distribution of inflammatory cells was decreased after LY333531 administration. Co-staining of CD68 and CD14 with CD11c showed that after excluding the influence of macrophages and monocytes, CD11c-labeled DCs had a significant reduction in plaques (i, j). Values, mean ± SED; n = 8; *p < 0.05 vs. ApoE + DM group; DM Diabetes mellitus, IL Interleukin, ICAM Intercellular adhesion molecule, VCAM Vascular cell adhesion molecule, TNFα Tumor necrosis factor alpha, IFNγ IFN gamma, AS Atherosclerosis, DAPI 4,6-diamino-2-phenyl indole