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Preface urotensin Ⅱ (urotensin Ⅱ, UT Ⅱ) the earliest from fishtail men pituitary extract neuropeptide, is known in vivo the strongest vasoconstrictor activity peptide. Its receptors are widely distributed in the mammalian heart, kidney, nerve tissue, vascular smooth muscle tissue, and even atherosclerotic plaques. UT Ⅱ in atherosclerotic play an important role in the development. This experiment, we observe dynamically change from normal rabbits until the pathogenic process in tail of vasopressin and its change with lipid inflammatory cytokines content to explore urotensin In a letter by copying rabbit atherosclerotic model atherogenic significance of sclerosis. Objective To study the arterial atherosclerosis model in UT II plasma levels of dynamic change, and their correlation with the blood lipoprotein inflammation factor analysis. Materials and Methods. Material health Japanese rabbits were 40, 4-month-old, male or female, were purchased from Shenyang Pharmaceutical University, Certificate of Conformity: SCXK (Liaoning) 2009-0002, weighing 2.0-2.5Kg. Formulated the basic diet of high fat diet, cholesterol (Sinopharm Chemical Reagent Co., Ltd., Shanghai production, AR), lard (commercially available), egg yolk powder (commercially available), three components were 0.6%, 3.3%, 8.3% ratio made, known as the high-fat diet. Experimental animal handling random rabbits were divided into two groups, the control group of 20 in the experimental group 20. Caged with drinking water ad libitum. Experimental rabbits fed a high fat diet, the control group continued to fed foundation rabbit feed. Each rabbit daily consumption of 150g, the experimental group to ensure that daily each rabbit eating cholesterol 1.0g, the lard 5.0g, egg yolk powder 12.5g. A total of 12 weeks feeding. Biochemical project detection experiment weeks, three weeks, six weeks, nine weeks, 12 weeks for blood specimens from plasma samples, serum TC, HDLC, LDLC level; enzyme-linked immunosorbent assay UT Ⅱ, IL-6 levels . While UT Ⅱ lipoproteins, inflammatory cytokines correlation analysis. Statistically analyzed using SPSS13.0 statistical software, comparison between groups using analysis of variance. Experimental results rabbit body weight after 12 weeks of feeding rabbits weight changes, changes in blood lipid content were increased, but no difference between the two groups (P gt; 0.05). The overall experimental rabbits lipid levels tended to increase. 6 weeks, compared with the control group, the average the experimental rabbits lipids water increases, the difference was statistically significant (P lt; 0.05), 12 weeks in rabbits with experimental group and 6 weeks of experimental rabbits, TC and LDLC significantly different (P lt; 0.01). 2 the rabbit plasma inflammatory cytokines UT Ⅱ and IL-6 levels, changes in high-fat diet fed rabbits in three weeks UT Ⅱ content in plasma began to decline, and 12 weeks were significantly reduced compared with the control group and six weeks visible, significant differences (P lt; 0.01). Inflammatory cytokines IL-6 levels began to rise in six weeks, but the difference was not statistically significance (P gt; 0.05), 9 and 12 weeks visible inflammatory factors were significantly higher in the control group and six weeks experimental group significant difference (P lt; 0.01) 3.UT Ⅱ with TC, UT Ⅱ TC serum IL-6 correlation analysis rabbits artery atherosclerosis model content was negatively correlated, r = -0.99, P = 0.01, linear regression equation Y = 0.211-0.003X. UT Ⅱ serum IL-6 levels showed a significant negative correlation, r = -0.95, P = 0.04, linear regression equation Y = 0.513-0.002X. Conclusion UT Ⅱ involved rabbits atherosclerosis hardening formation process, and the serum containing gradually reduced. Their lipid levels, inflammatory cytokines IL-6 serum level was negatively correlated. Lipid levels significantly increased in the process of atherosclerosis formation, most significantly elevated total cholesterol. The inflammation reaction throughout the formation of atherosclerosis always and in which UT Ⅱ interaction, and ultimately lead to atherosclerosis formation.
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