| Objective Based on establish a rat model of traumatic limbs deep vein thrombosis (DVT) ,gene chip technology will be utilized to detect the femoral vein wall genes expressional variations in traumatic DVT (TDVT). Then to analyze the differential expression genes in the two pathologic states of thrombosis occurrence and no occurrence at crest-time of TDVT, and so as to screening the juncture genes and molecule markers related to TDVT.Materials and Methods 1,Grouping: 10 SD rats were selected randomly from 150 for normal control group (group A, n=10) According to different phases after model being built, the other 140 SD rats were divided into 7 groups: trauma instant group (B), thrombosis prophase group (C), thrombosis and non-thrombosis groups (D and H) at crest-time group , thrombi resolution group (E), thrombi insolution group (F), non-thrombosis group all the time (G).2,Modelling: Through beat on bilateral posterior limbs (1cm long under greater trochanters) and hip spical cast fixation to establish TDVT rat model. Group A rats were not beat. The traumatic energy is 5J. Rat hibateral posterior limbs were fixed with hip spica casts except for group A and B.3,According to different phases after model being built, rats were anesthetized with 3% pentobarbital sodium (1ml/kg, intraperitoneal injection),supine position fixation,sterilization, exposing hibateral femoral veins and the major tributaries. In group A, 4～5cm femoral vein and related main tributaries were resected. In group B, at 0．5h; group C, at 72h; group D and H, atl20h; group E, F and G, at 168h after model being built, the same region vascular tissue was also resected separately. Part of the proximal vessel (0．5 cm long, approximately) separated for histological analysis, the other vessels were rinsed by 0．9% physiological saline;The vessel specimens were put into nitrogen canister in less than 30 seconds after ex vivo, which would be used for total mRNA extraction.4,Through TRIzol method, total mRNAs of femoral vein specimens were extracted separately. After all the total mRNAs samples were checked by agarose gel electrophoresis, according to the operation flowsheet of Genechip Rat Genome 230 2．0 gene chip, cDNA probes preparation, hybridization, washing, staining and scanning were performed orderly to finish array detecting. All data were analyzed and summarized. The expression genes were analyzed by Fold Change analysis and Go functional classification. Cluster analysis. Then used cluster method to analysis the differential expression genes in the group D and H at crest-time of thrombosis.Results 1．In the 150 rats, total 5 rats died. The reasons for the died are as follows: 8 rats owing to hemorrhagic shock, 7 rats due to infection, and the other 3 due to anesthetic accident.2．In this study, the mortality of rats is 12%; the rate of thrombosis at 120h is 50．6%; the rates of thrombus resolution and insolution at 168h is 56．7% and 43．3% respectively; the rate of non-thrombosis is 44．6%.3．The 8 total RNA samples were approved to be high qualities without degradation. The hybridization signal intensity of arrays was satisfactory, the results were reliable.4．In the 31042 rat genes which can be detected by Genechip Rat Genome 230 2．0 microarray. In BvsA,349 displayed differential expression:214 were up-regulated, 135 were down-regulated; In CvsA,2393 displayed differential expression: 1386 were up-regulated, 1007 were down-regulated; In DvsA,1743 displayed differential expression:945 were up-regulated,798 were down-regulated; In HvsA,2790 displayed differential expression:1685 were up-regulated,1105 were down-regulated; In EvsA,1913 displayed differential expression: 1222 were up-regulated,691 were down-regulated;In FvsA,2564 displayed differential expression: 1535 were up-regulated, 1029 were down-regulated; In GvsA,1849 displayed differential expression: 1235 were up-regulated,614 were down-regulated. In DvsH, the differential expression genes were 805, 51 were up-regulated and 755 were down-regulated. The functions of all differential expression genes were involved in apoptosis, molecule binding, metabolism, cell cycle and signal transduction, etc.5．In DvsH, 195 were obvious differential expression genes (Signal Log2 Ratio≥2 and Signal Log2 Ratio≤-2) , in which 5 were up-regulated and 190 were down-regulated. The functions of these genes included fibronolysis, signal transduction, the proliferation, differentiation and apoptosis of cells, cytoskeleton, motion and migration of the vascular smooth muscle, etc.6．The obvious differential expression genes in DvsH were analyzed by Cluster analysis. There were three groups of genes that present the coexpression trend.①The co-expression genes with Plaur: there were Jun, Junb, Btg2, RGD1310800_ predicted, RGD1307235_ predicted, Eif4ebp2_predicted, 1377117 _at, 1398620_at;②The co-expression genes with Plaur were Dusp1, Mylk, Cebpd, Glg1, Kns2, Usf2, Ccnd2, Cdhl3, Itga1, Nedd4a, Igsf4b_predicted, Snxllpredicted,RGD1308805_predicted, 1374974_at,1393167_at,1379897_at,1371329_at,1385925_at,1385704_at,1392361_at,1382565_at,1375362_at,1390116_at;③The co-expression genes with Timp3 were Gna15,Lasp1Conclusions 1．The femoral vein wall differential expression genes are mainly related to fibrolysis, cell apoptosis, molecule binding, metabolism, cell cycle and signal transduction, etc, it suppose that these biological processes are play an important role in TDVT.2．The obvious differential expression genes at the crest-time of thrombosis are relevanted to apoptosis and molecule adhesion; 5 genes in DvsH are obvious up-regulated, there are Serpinb2, Rn.18307 ,Rn.32617,Rn.l36393,1377655_at, except for Serpinb2,the function of other 4 genes were unknown, it is essential to confirm it.3．PAI-1 and Plaur are play an important role in traumatic deep vein thrombosis through mediated the expression of t-PA and u-PA.4．4 co-expression genes with PAI-1 are 1377117_at,RGD1310800_ predicted,RGD1307235_ predicted,1398620_at, the biological function of these genes were unknown, their could be inhibit the process of fibrinolysis.
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