LAUSR

BACKGROUND Hemorrhagic shock (HS) is the most common cause of potentially preventable death after traumatic injury. Acute liver injury is an important manifestation of HS. Apoptosis plays an important role in liver injury. Farnesoid X receptor (FXR) can alleviate liver injury. We designed this experiment to study the effects of ursodeoxycholic acid (UDCA) on hepatocyte apoptosis in HS and its relationship with the FXR pathway. METHODS Mice were randomly divided into 4 groups: sham group; HS group; HS + UDCA group and FXR (-) + HS + UDCA group. There were 6 mice in each group. As to model of HS, MAP of 40 ± 5 mmHg was maintained for 1 hour. As to UDCA intervention, UDCA (300mg/kg) was given nasally fed. Real-time RT-PCR, Western Blotting are used to detect changes of the expression level of caspase-3, bax, LC3Ⅰ, LC3Ⅱ, bcl2 and beclin1 in liver. TUNEL are used to detect changes of hepatocyte apoptosis. RESULTS The expression level of caspase-3 and bax in liver decreased significantly after treatment with UDCA under HS conditions. The expression level of LC3Ⅰ, LC3Ⅱ, bcl2 and beclin1 in liver increased significantly after treatment with UDCA under HS conditions. TUNEL positive percentage of liver decreased significantly after treatment with UDCA under HS conditions. In the case of FXR (-), the influence of UDCA was inhibited. CONCLUSIONS These results indicate that UDCA can reduce hepatocyte apoptosis during HS through the FXR pathway.