Abstract
Purpose: Carotid atherosclerosis is a serious vascular disease, leading to various cerebrovascular diseases. Methods: Gene expression profile of GSE100927 was selected to conduct differentially expressed genes. Then we performed protein-protein interactions, Gene ontology, and Kyoto Encyclopedia of Genes and Genomes analysis. Then we used HUVEC, HAVSMC, and THP-1 induced macrophages cells to conduct experimental verification. The experimental groups were as follows: Control group, Solvent control group, and Palmitic acid group. We measured the levels of reactive oxygen species in three cells via flow cytometer or fluorescence microscope. Then we detected apoptosis of HUVEC cells and HAVSMC cells or observed nucleus of THP-1 induced macrophages cells. Results: We selected male carotid atherosclerosis, with 10 control samples and 21 atherosclerosis samples. The results of pathway enrichment showed that “Toll-like receptor signaling pathway” ranked first. We chose IL1β, CCL4, SPP1, CCL3, IRF5. MMP7 and MMP9 for experimental verification. Palmitic acid increased the reactive oxygen species levels and the apoptosis rates of HUVEC cells and HAVSMC cells while increasing the activity of THP-1 induced macrophages cells, and it cannot increase the level of reactive oxygen species, and shrink the nucleus. Palmitic acid increased mRNA levels of IL1β, CCL4, SPP1, CCL3, IRF5. MMP7 and MMP9 in HUVEC cells and THP-1 induced macrophages, and increased the mRNA levels of CCL4 and MMP9 in HAVSMC cells,not changed the mRNA level of IRF5. Conclusion: IL1β,CCL3, CCL4, SPP1, IRF5, MMP7, and MMP9 are significant markers of carotid atherosclerosis.