关键词: 不规则趋化因子, CX3CR1, 核因子-κB, 肿瘤坏死因子, 卡托普利

Abstract: Objective By researching the effects of G-coupled protein on the expressions of nuclear factor kappa B(NF-κB) and tumor necrosis factor-α(TNF-α) in peripheral blood monocytes induced by fractalkine(FKN) to explore one of possible signal conductive mechanisms of FKN/CX3CR1 and the invention of captopril.Methods Peripheral blood monocytes were isolated from fresh blood of healthy volunteers by Ficoll-Paque gradient centrifugation and divided into control group,FKN group,G-protein inhibitor pertussis toxin(PTX)group,PKC inhibitor RO31-8220 group,inhibitor NF-κB PDTC group,captopril group;the expressions of NF-κB in monocytes from each group were measured by immunohistochemsitry; the supernatant of monocytes was collected from each group,the expressions of TNF-α were dete rmined by enzyme-linked immunosorbent assay(ELISA).Results The expressions of NF-κB and TNF-α in FKN group were increased compared with control group(P<0.05);the expressions of NF-κB and TNF-α in G-protein inhibitor PTX group were decreased compared with FKN group(P<0.05);the expressions of NF-κB and TNF-α in PKC inhibitor RO31-8220 group were decreased compared with FKN group(P<0.05);the expression of TNF-α in NF-κB inhibitor PDTC group was decreased compared with FKN group(P<0.05);the expressions of NF-κB and TNF-α in captopril group were decreased compared with FKN group(P<0.05).Conclusion FKN-CX3CR1 increases the expressions of NF-κB and TNF-α in peripheral blood monocytes;Captopril participates in inhibiting inflammatory and preventing arteriosclerosis perhaps by reducing the expressions of NF-κB and TNF-α in peripheral blood monocytes induced by FKN-CX3CR1;one of signal conductive mechanisms of FKN-CX3CR1 contributing to the progression of atherosclerosis is the following series of cascaded reaction:FKN-CX3CR1→G-coupled protein→PKC→NF-κB→TNF-α.

Key words: fractalkine, CX3CR1, nuclear factor-κappaB, tumor necrosis factor, captopril