LAUSR

Objective Verification the changes in expression and mechanism of serum inflammatory factor IL-1 beta and related biomarkers by establishing an animal model of deep vein thrombosis (DVT) in lower extremity of rats. Methods Seventy male SPF SD rates, weighing (200±20) g, randomly divided into groups of ten and made each group of rats equal in weight. Recorded as control group, sham operation group, model experiment 2, 8, 24, 48, 72 h group. The control group was fed normally without any treatment; the sham operation group, laparotomy was performed without vein ligation; the model experimental group was divided into different groups according to different time periods. The model of venous thrombosis of lower extremities was established through venous ligation surgery in rats, they were sacrificed at the 2 hours, 8 hours, 24 hours, 48 hours and 72 hours after the modeling, and blood samples and tissues were collected. The expression levels of IL-1β, tissue factor and xanthine oxidase (XOD) in blood samples of 7 groups of rats were measured by ELISA. DVT morphology were analyzed by Pathology, flow cytometry were used to count peripheral blood circulating endothelial cells in rats separated after injury. The expressions of IL-1β, tissue factor, XOD, pathological and flow results were compared between the normal control group, the sham operation group and the lower extremity deep vein thrombosis model group at different time periods. All data were represented by mean standard deviation (Mean±SD). One-way anova was performed on the measurement data, and the LDS method was used to compare the two pairs. The test level was α=0.05. Results IL-1β, tissue factor, XOD showed no significant difference between the control group and the sham operation group, P>0.05. The model experimental group showed an upward trend in the process of 2 h-24 h and reached a peak value at 24 h. The histopathology showed that red thrombus and mixed thrombus could be seen within 2 h-48 h in the thrombosis model experiment group. The blood vessel wall was accompanied by inflammatory cell infiltration. After 72 h, the thrombus was obviously organized. The CD31 concentration of the control group and the sham operation group were (4.04±1.00), (4.82±1.12), and the difference between the two difference between the two groups was not statistically significant (P<0.05); the CD31 concentration of model experimental group had significant differences from 2 h, (5.188±0.895); 8 h, (5.614±1.243); 24 h, (9.785±1.996); 48 h, (14.198±2.172); 72 h, (18.118±1.025), it continued to increase, P<0.05. Conclusion High expression of inflammatory IL-1β and related markers tissue factor, XOD confirmed the mechanism of injury of deep venous endothelial cells in lower extremities caused by IL-1β and the mechanism of further aggravation of thrombosis after injury. Key words: Venous thrombosis; Interleukins; Inflammation; Circulating enelothelinal cells