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Test Background: With the in-depth study of atherosclerosis pathogenesis , recently discovered inflammatory endothelial release of a new chemokine fractalkine (FKN) can promote inflammation , the FKN its receptor CX3CR1 binding , can lead to the Gi protein even associated with signal transduction , the expression of the receptor of natural killer (NK) cells to enhance the lethality of NK cells in a dose - dependent manner , resulting in the injury of vascular endothelial cells . While the expression of the receptor of monocytes, lymphocytes, etc. generated directional migration signal to vascular endothelial cells , chemotaxis, adhesion, thereby promoting the formation of atherosclerosis . FKN-CX3CR1 signaling mechanisms affect atherosclerosis formation process in the study , we found that there may be a series of cascade FKN-CX3CR1, G- protein , PKC, NF -κB , TNF -α , and so the purpose of this experiment is to explore these five between the upstream and downstream relationships and their impact on atherosclerosis , and captopril, which may play a role in regulation . Test purposes : ( 1 ) to explore the FKN-CX3CR1 to affect atherosclerosis signaling mechanism . (2 ) study the role of G-protein to affect atherosclerosis signaling mechanism FKN-CX3CR1 . ( 3 ) studies of PKC in FKN-CX3CR1 affect the role in atherosclerosis signaling mechanisms . ( 4 ) affect atherosclerosis signal transduction mechanisms of NF-κB in FKN-CX3CR1 . (5) captopril FKN-CX3CR1 to affect atherosclerosis signal conduction mechanism of intervention . Test Method: FKN G -protein blocker PTX , PKC inhibitors RO31-8220, NF-KB blocker PDTC , Captopril -induced human peripheral blood mononuclear cells , and then applying immunohistochemical techniques to detect cell expression of NF-κB , TNF-α secretion by enzyme-linked immunoassay technology to detect cell .
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