Fig. 4
PKCβ1 inhibitors significantly inhibited the immune maturation of DCs. PKCβ1 inhibitors significantly down-regulated the expression of CD83 and CD86 in BMDCs, as well as the inflammatory cytokines, TNFα and IFNγ, tested by ELISA. However, PKCα inhibitors and PKCβ2 inhibitors did not have similar effects (a, b, *p < 0.05 vs. oxLDL + AGEs group). PMA, a PKC agonist, up-regulated the expression of CD83 and CD86 in BMDCs and promoted the secretion of the inflammatory cytokines, TNFα and IFNγ, while PKCβ1 inhibitors inhibited these effects (c, d, *p < 0.05 vs. control group; #p < 0.05 vs. PMA group). PKCβ1 inhibitors inhibited the PMA− and oxLDL plus AGEs-induced activation of the NF-κB signaling pathway (e, f, *p < 0.05 vs. oxLDL + AGEs group). Values, mean ± SED; n = 3, oxLDL oxidized low density lipoprotein, AGEs advanced glycation end-products, PKC protein kinase C, IFNγ IFN gamma, TNFα Tumor necrosis factor alpha, PMA phorbol ester, NF-κB nuclear factor-κB