Abstract: 【Abstract】 Objective To explore the mechanism of preterm birth (PTB) induced by placental injurycaused by lipopolysaccharide (LPS). Method Pregnant CD1 mice were utilized and randomly divided tocontrol group (n=16) and LPS group (n=24). At the seventeenth day of gestation (E17), pregnant mice weretreated by intrauterine injection of 25 μg LPS for LPS group or 100 μl phosphate buffered solution (PBS)for control group. At 6 h and 24 h after injection respectively, placental samples were collected in controlgroup (n=5) and LPS group (n=6). At 24 h after injection (E18), the weight of fetal mice was recorded. Inthe retained 12 mice in LPS group and 6 mice in control group, the PTB (were compared. Hematoxylin and eosin (HE) staining and vimentin immunofluorescence staining were usedto observe the placental structure. Real-time quantitative polymerase chain reaction (PCR) was applied fordetecting the mRNA levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α). Westernblotting was employed to measure the protein levels of phosphorylated and total nuclear factor kappa-B(NFκB). Student's t test and χ2 test were used to perform statistical analysis. Result The rate of PTBin LPS group was 75.0% (9/12) and there was no PTB in control group. The total survival rate of fetalmice in LPS group was significantly lower than that in control group [27.8% (42/151) vs 96.2% (75/78),χ2=96.127, P<0.001]. The weight of fetal mice at 24 h after injection (E18) in LPS group was significantlylighter than control group [(1.35±0.12) vs (1.69±0.05) g, t=5.996, P<0.001]. At 6 h after injection, incontrast to control group, placental labyrinth zone in LPS group had loose structure, increased organizationalgaps, less infiltration of blood cells and decreased vimentin distribution. At 24 h after injection, the structureof labyrinth zone was unchanged in LPS group. Additionally, at 6 h after injection, the mRNA levels of IL-1β(0.307±0.175 vs 0.020±0.014, t=3.611, P=0.006), IL-6 (0.223±0.189 vs 0.004±0.002, t=2.956, P=0.032)and TNF-α (0.25±0.16 vs 0.06±0.02, t=2.684, P=0.025) in LPS group were significantly higher than thosein control group. At 24 h after injection, the mRNA levels of IL-1β (0.045±0.035 vs 0.009±0.006, t=2.292,P=0.048) and IL-6 (0.020±0.016 vs 0.002±0.001, t=2.413, P=0.039) in LPS group were higher than those in control group, but there was no statistical difference of the TNF-α mRNA level (0.10±0.06 vs 0.07±0.04, t=1.071, P=0.312) in LPS group and control group. At 6 h after injection, the relative protein expression of phosphorylated NFκB in LPS group was significantly higher than that of control group (1.23±0.48 vs 0.66±0.13, t=2.569, P=0.030). Conclusion After pregnant mice are exposed to intrauterine inflammationcaused by LPS, the placentas appear structure injuries induced by inflammation. The obvious injury in placentaat early inflammatory stage may be one of the important causes responsible for PTB and stillbirth