| At present, cardiovascular is the major disease that threaten the people’s health around the world, and atherosclerosis is one of the most important cardiovascular diseases. The inflammatory response plays a significant role in the pathogenesis of atherosclerosis (AS). Oxidized LDL (ox-LDL) induces endothelial cell (EC) dysfunction and smooth muscle cell (SMC) proliferation, and the promotion of the inflammatory response is considered to be important risk factors involved in atherosclerosis. The formation of atherosclerosis (AS) has a great relationship with fatty acid intake and type. Many studies have shown that triglycerides were closely related to the occurrence and development of cardiovascular diseases, especially atherosclerosis.At first, this research investigated the influence of tristearin, triolein and trilinolein on the proliferation model of human umbilical vein smooth muscle cells (HUVSMC) induced by oxidized low-density lipoprotein (ox-LDL), Methyl thiazolyl tetrazolium (MTT) assay was used to determine the proliferation and cell growth curve of HUVSMC, crossed wound healing assay was used to determine the influence of Triglycerides (TG) on the ability to migrate of HUVSMC. Finally, western blotting was used to determine the influence of triglycerides (TG) on the protein expression of PCNA, a-actin and MCP-1in smooth muscle cells, and quantitative PCR was used to determine the influence of triglycerides (TG) on the m-RNA expression of PCNA, SM-a-actin, MCP-1protein in smooth muscle cells, which indepth analysed the mechanisms of different acylation positional triglycerides in atherosclerosis. The main findings of this research were as follows1. The tristearin had a promotion effect on the HUVSMCs induced by ox-LDL, the promoting rate increases with the increase of time and has a positive correlation with the concentration of the drug; Triolein and trilinolein could inhibit the proliferation of the HUVSMCs, the inhibition rate increased with the increase of time and the inhibition rate was positively correlated with the concentration of50-500 μmol/L.2. Significantly, Tristearin could increase the SFA content in SMC, while the MUFA and PUFA content reduced with a corresponding reduction of n-3and n-6fatty acids content. Triolein could cause slight increase of SFA, significant increase of MUFA and reduction of PUFA, while there was no significant change in n-3and n-6fatty acid content. Trilinolein caused significant reduction of SFA and increase of PUFA, MUFA showed no significant change, n-3and n-6fatty acid content increased.3. The tristearin could promote the migration of SMCs induced by ox-LDL, while the triolein and trilinolein had inhibitory effects, and the inhibition of trilinolein was a little weaker than the triolein’s.4. Using the tristearin to treat the SMCs induced by ox-LDL for48h, the protein expression related to cell proliferation and cell cycle changed. Compared with ox-LDL group, treatment with Tristearin on ox-LDL-stimulated increased the expression of PCNA and MCP-1, as well as the mRNA, the SM-a-actin protein and mRNA expression downregulated. Otherwise, treatment with Triolein and Trilinolein on ox-LDL-stimulated negatively affected the expression in protein and mRNA of PCNA and MCP-1, while SM-a-actin protein and mRNA expression upregulated.The results show that, tristearin had significant promotion effects on the proliferation and migration of the smooth muscle cells induced by ox-LDL. The induction effect rendered dependence of time and dose, which had a definite enhancing effect on the atherosclerotic process. While the triolein and trilinolein could inhibit the proliferation of the smooth muscle cell induced by ox-LDL, reduce cell migration distance and had certain inhibition of the atherosclerotic process. |
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