Objective　　　 To explore the changes of glucose-regulated protein78 (GRP78) and C/EBP homologous protein (CHOP) in rat model of endoplasmic reticulum stress during septic shock and its relationship with pulmonary vascular permeability.　　　 Methods　　　 A t

otal of 42 adult SD rats

with half females and half males weighing 200 to 220 g

were randomly divided into 3 groups

sham-operation group (n=6)

cecal ligation and puncture (CLP) group

CLP plus taurine group (5 mL/kg taurine through intravenous injection immediately before CLP establishment

n=6). CLP group was further divided into 5 subgroups

in 1

2

4

6 and 8 h respectively after CLP

each subgroup having 6 rats. After fluorescein isothiocyanate-labeled albumin bovine serum was injected intravenously

lung tissues of rats were taken at above time points after CLP in CLP group

and at 6 h after CLP in CLP plus taurine group. The pulmonary vascular permeability was determined by observing the permeability of fluorescein. The expression of GRP78 and CHOP in pulmonary vascular endothelial cells were determined by Western blotting.　　　 Results　　　 The expression of GRP78 and CHOP at protein level were also increased in a time-dependent manner after CLP (

P

0.05).The permeability of fluorescein was in a straight line up in a time-dependent fashion after CLP as compared to sham-operation group （

P

0.05）. The expression of GRP78 and CHOP was positively correlated with the changes of vascular permeability（

R

2

=0.785

P

0.05; R

2

=0.881

P0.05）. Taurine intervention resulted in significantly decreased permeability of fluorescein compared with CLP group （

P

0.05）

and significantly decreased expression of GRP78 and CHOP （

P

0.05）.　　　 Conclusion　　　 Endoplasmic reticulum stress during septic shock participates in the increase of vascular permeability

and GRP78 and CHOP are important participating molecules.