Objective In the present study, the effect of Fractalkine (FKN) on the expression of NF-κB and TNF-α induced by FKN was investigated one of possible signal transduction pathways of FKN/CX3CR1 in atherosclerosis, and the role of PI3K were also investigated.
Methods 1) Peripheral blood monocytes were isolated from fresh blood of healthy volunteers by Ficoll–Paque gradient centrifugation. 2) Divide the extractive peripheral blood monocytes into four groups :control group, FKN group, LY294002 group and PDTC group. 3) Measure the NF-κB expression of monocytes from each group by Western Blot. 4) Collect the supernatant of monocytes from each group, determine the expression of TNF-α by ELISA.
Result 1. The expression of NF-κBand TNF-αin FKN group was increased, compared with that control group (p<0.05). 2. The expression of NF-κB and TNF-α in LY294002 group was decreased, compared with that FKN group (p<0.05).
Conclusions FKN-CX3CR1 increase the expressions of NF-κB and TNF-α in peripheral blood monocytes, which may be one of the mechanisms of contributing to the progression of atherosclerosis; After interacting with its receptor CX3CR1, FKN activates the PI3K by coupled with G-protein and then initiates intracellular signal conductive mechanism.
- nuclear factor-κB
- tumour necrosis factor–α