Aim Using animal model to determine the effect of recombinant human tumor necrosis factor-like weak inducer of apoptosis （rhTWEAK） on aortic endothelial diastolic function and tissue factor and its inhibitor. Methods C57BL mice were randomly divided into four groups: （1）rhTWEAK group: given rhTWEAK by intraperitoneal injection （2）rhTWEAK＋anti-rhTWEAK group: after intraperitoneal injection with anti-TWEAK factor, then treated with rhTWEAK factor 15 minutes later （3）IgG group: treated with nonspecific IgG （4）Control group: given the same amount 0.3 mL of normal saline injection. After 7 weeks, we took eyeball blood to separate supernatant and thoracic aortic area to detect the vasodilatation function. Circulating endothelial nitric oxide synthase （eNOS）, high-sensitivity C-reactive protein （hs-CRP）, nitric oxide （NO） and tissue factor （TF） and tissue factor pathway inhibitor （TFPI） were detected in mouse plasma by enzyme linked immunosorbent serologic assay. Results （1）We found that endothelial diastolic function and the concentration of NO and eNOS in plasma in TWEAK group obviously decreased, TF levels increased significantly and the TFPI decreased when compared with control rhTWEAK＋anti-rhTWEAK and IgG group, those factors had significant difference （P<0.05）, however the hs-CRP content had no obvious change （P>0.05）. （2）Our results show that the endothelial diastolic function and the content of NO eNOS TF and TFPI and hs-CRP have no obvious difference in the control rhTWEAK＋anti-rhTWEAK and IgG group （P>0.05）. Conclusion rhTWEAK can induce endothelial dysfunction and blood coagulation factor content changes, and this may be a mechanism of vascular endothelial damage in early stage atherosclerosis.