Objective To observe the mechanism of curcumin （C UR） for lung tissue injury in acute pulmonary embolism （A PE） rats.Methods Totally 96SD rats were randomized into the normal group

sham group

model group

low-dose CUR group

middle-dose CUR group and high-dose CUR group

with 16in each.The APE models were established by injecting self-thrombus.The low-dose CUR group

middle-dose CUR group and high-dose CUR group was given 50mg /kg

100mg /kg and 200mg /kg of CUR respectively.The normal group

sham group and model group was given the same volume of saline.The rats were given intragastric administration 40minutes and 24hours before modeling and once daily after modeling.The rats were sacrificed on the 4hand 72hafter modeling.The serum levels of interleukin-8 （IL-8）

tumor necrosis factor-α （TNF-α） and interleukin-1 β （IL-1 β） were measured with enzyme-linked immunosorbent assay （E LISA）.The pathological changes of lung tissue were observed with HE staining.The Chemokine （C-X3-C motif） ligand 1 （C X3CL1） and CX3Cchemokine recep-tor 1 （C X3CR1） levels in lung tissue were measured with immunohischemical method.Results The IL-8levels in the normal group

sham group

low-dose CUR group and middle-dose CUR group were significantly lower than those in the model group on the 4hand 72hafter modeling （P<0.05or P<0.01）.The TNF-αlevels in the normal group

sham group and high-dose CUR group were significantly lower than that in the model group on the 72hafter modeling （P<0.05）.The IL-1 β levels in the normal group

sham group

low-dose CUR group

middle-dose CUR group and high-dose CUR group were significantly lower than that in the model group on the 72hafter modeling （P<0.05）.On the 72hafter modeling

the hyperemia of the lung tis-sues was apparently reversal after applying CUR.The CX3CL1-postive cell counts in the normal group

sham group and high-dose CUR group were significantly lower than those in the model group on the 4hafter modeling （P<0.01）.The CX3CR1-postive cell counts in the normal group

sham group

middle-dose CUR group and high-dose CUR group were significantly low-er than those in the model group on the 4hafter modeling （P<0.01）.The CX3CL1-postive cell counts in the normal group

sham group

low-dose CUR group

middle-dose CUR group and high-dose CUR group were significantly lower than those in the model group on the 72hafter modeling （P<0.05or P<0.01）.The CX3CR1-postive cell counts in the normal group and sham group were significantly lower than those in the model group on the 72hafter modeling （P<0.01）.Conclusion The in-flammatory response appears in APE rats.CUR can inhibit the levels of IL-8

TNF-α

IL-1 β

CX3CL1and CX3CR1in APE rats

which may be relevant to relieving lung tissue injury.