[Objective] to investigate whether intestinal expression of Toll-like receptor 4 (TLR4) signaling was involved in bacterial translocation and mediated sepsis generation in a rat model of cardiopulmonary resuscitation (CPR). [Methods] Through the establishment of rat model of CPR

the experimental animals were set CPR-6 hour group (CPR-6h) and CPR-48 hour group (CPR-48h) as the early and late stages after the establishment of spontaneous circulation

then observed two-stage intestinal TLR4 expression and MAPKs(pERK

pJNK and pp38MAPK) expression of intracellular signaling proteins by using western blot

detected bacterial translocation by bacterial culture of mesenteric lymph nodes (MLNs) and liver tissue

determinated intestinal epithelial damage by observing cell junction widening or opening ratio. [Results] In the CPR-6h group

TLR4

pERK

pJNK

pp38MAPK protein expression were significantly increased (P<0.05

compared with sham control)

and a low percentage of cell junction widening or opening ratio (2.01%) and a small quantity of colonies of colony-forming unit per gram (cfu/g ) were observed in the mesenteric lymph nodes (MLNs) and liver tissue. However

in the CPR-48h group

except for pERK

TLR4

pJNK and pp38MAPK protein were decreased

which were compared with those in the CPR-6h group (P <0.05). However

the percentage of cell junction widening or opening ratio was much higher than that in the CPR-6h and sham groups (8.4%

P<0.001). Moreover

the bacterial colonies of mesenteric lymph nodes and liver tissue were （14300±2750）cfu/g and（4400±623）cfu/g

which were remarkably increased when compared to CPR-6h groups [(3700±1090)cfu/g and （9800±850）cfu/g

P<0.001]. [Conclusion] The lower expression of intestinal mucosal TLR4 signal was observed during the late stage of CPR

which suggested that intestinal mucosal cells may reduce its ability to sense and identify bacteria

which resulted in bacterial translocation.