The Research Of CD8+T Lymphocytes In Atherosclerotic Plaque

Background and purpose:With the improvement of living standards and the change of social labor, the morbidity and mortality rates of atherosclerosis increase year by year, which has become the top killer to human health, affecting people's quality of life seriously, and causing great mental burden and economic burden. Although medical level and treatment improved, it is difficult to cure the disease. Recently, it was reported that there are a lot of T lymphocytes in atheromatous plaques, and since then, the relationship between atherosclerosis and immune mechanism were more and more concerned. There are few reports about the (?)ole of CD8+T lymphocytes in atherosclerosis. The trend of expression of CD8+T lymphocytes in atherosclerosis remains absurd.This research mainly explores the role of CD8+T,MMP-9, and OX-LDL in atherosclerosis through testing their expression in atherosclerosis process. In recent years, it was found that OX-LDL play a very important role in process of atherosclerosis formation, especially in ApoE gene knockout mice atherosclerosis model, the OX-LDL promote atherosclerosis formation obviously. MMP-9 is an important member of the matrix metalloproteinase family, which play key roles in damage reactions and atherosclerosis (AS) formation process. They could biodegrade basement membrane collagen and lead to the occurrence of acute coronary syndrome.Methods:Establish atherosclerosis sclerosis mice model.28 Laboratory mice,16 of them for Apoe gene knockout (Apoe-/-) mice,10 of which were randomly divided into a high-fat diet group (Ah), and the rest 6 mice were normal diet group (An). Another 12 C57BL/6 mice were homologous to knockout mice. Six of them were randomly divided into a high-fat diet group (Ch) and 6 mice were normal diet group (Cn). Ah group and Ch mice were given high-fat diet for 12 weeks. Then, we picked eye to take some blood serum from empty stomach mice, then killed them and get aorta to observe atheromatous plaque formation conditions. We observed pathological change under light-microscopy after Aortic specimen for HE dyed, and detected the concentration of MMP-9, CD8, OX-LDL in atheromatous plaque using immunohistochemical method, measured the mean gray degree of the immune deposits of MMP-9, CD8, OX-LDL in aortic endometrial and measured MMP-9 and ox-LDL level in the plasma of mice using the method of ELISA.Results:General form of Atherosclerosis plaques in gross:Ah mice atherosclerotic plaque formation is mainly concentrated in arterial plaque bifurcation place. The quantity of plaques is medium. There are patches on the abdominal aorta in some of the mice. There is no atherosclerotic plaque formation in An and Cn group mouse. Neither in Ch group mice, but the fat content in peritoneal and organ surface are significantly increased. The result of HE stain showed the plaques formation and foam cells in Ah groups are more than Cn group. The plaques formation and foam cells in Ch groups are more than normal group, but in a lesser degree. Endometrium is smooth in An group which is exactly the same as the normal group. Immunohistochemical stains show that in An group: the expression of MMP-9 is more than control group, but no statistical significance,P>0.05. MMP-9 expression in Ch group is more than control group, P<0.01. MMP-9 expression in Ah group is more than control group, P<0.01. The result of comparing MMP-9 expression in different groups is CnCh>An>Cn. The concentration of OX-LDL in An group is more than Cn group, which is no statistically significant, P>0.05. OX-LDL level in Ch group is more than Cn group, P<0.01, statistically significant. Comparing of OX-LDL level in different groups is:Ah>Ch>An>Cn. It was statistically significant between these groups.Conclusion:In the model of mice atherosclerosis, with the patch quantity and foam cells increasing, CD8+T lymphocytes are diminished.In mice models of atherosclerosis, MMP-9 is positive related with progression of atherosclerosis degree. In mice models of atherosclerosis, OX-LDL promotes the progression of atherosclerosis degree.