Effects of oxidative stress and Rac1/2 on venous wall and their roles in traumatic deep vein thrombosis******☆

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Abstract

BACKGROUND:

The molecular mechanism and core regulatory network of deep vein thrombosis are not fully clarified yet.

OBJECTIVE:

To explore the roles of oxidative stress and Rac1/2 in rat deep vein thrombosis.

METHODS:

Deep vein thrombosis model in SD rats was established by a champing method femoral veins clamping combined with fixation of the lower extremity with plaster. The incidence and serious degree of thrombus were observed by dissecting rat femoral vein at different time points (2.5 and 25 hours after modeling). The model rats were divided into pre-thrombogenesis group (2.5 hours after modeling), thrombogenesis group (25 hours after modeling) and non-thrombogenesis group (25 hours after modeling). Then total RNA and protein were extracted from the femoral venous wall tissues.

RESULTS AND CONCLUSION:

Colorimetry results showed that compared with the non-thrombogenesis group, the concentration of malondiadehyde in rat femoral vein wall tissues of the thrombogenesis group was the highest (P < 0.05), followed by that of the pre-thrombogenesis group (P < 0.05). The concentrations of total superoxide dismutase and glutathione reductase in the thrombogenesis group were the lowest, followed by those in the pre-thrombogenesis group (P < 0.05). The results of gene chip hybridization analysis and real-time PCR showed that compared with the non-thrombogenesis group, the expressions of Rac1 and Rac2 in rat femoral vein wall tissues of thrombogenesis group increased the most, followed by that of the pre-thrombogenesis group (P < 0.05). These findings indicate that the up-regulation of malondialdehyde and Rac1/2 as well as the activity decrease of total superoxide dismutase and glutathione reductase may lead to the formation of deep venous thrombosis.

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