Mesenteric lymph duct ligation relives hepatic injury subjected to two-hit in rats
- VernacularTitle:肠系膜淋巴管结扎减轻二次打击所致大鼠肝损伤
- Author:
Geng ZHANG
;
Junxu REN
;
Zigang ZHAO
;
Yuping ZHANG
;
Chunyu NIU
;
Jing ZHANG
- Publication Type:Journal Article
- Keywords:
mesenteric lymph duct;
ligation;
liver injury;
two-hit;
inflammatory mediators
- From:
Basic & Clinical Medicine
2006;0(10):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of mesenteric lymph duct ligation relieving hepatic injury in rats by two-hit of hemorrhage and LPS.Methods Forty-five Wistar rats were divided into three groups: ligation group,non-ligation group and sham group,and the two-hit model was established by hemorrhage and LPS,mesenteric lymph was blocked by ligating mesenteric lymph duct in ligation group.After 24 hours of operation,took out the liver for pathological section,and the hepatocellular apoptosis rate was determined by method of TUNEL,the expression of BCL-2 and BAX protein was determined by immunohistochemical test.At the same time,taking out liver for homogenate of 10 percent,the activity of MPO and ATPase and the contents of TNF-? and IL-6 were determined in hepatic homogenate.Results After two-hit,the hepatocellular apoptosis rate and expression of BAX protein in non-ligation group were significantly increased as compared with sham group and ligation group,and expression of BCL-2 protein was significantly lower.The contents of MPO,TNF-? and IL-6 in hepatic homogenate of non-ligation group were significantly increased than that of sham group,and the activity of ATPase in hepatic homogenate was significantly lower.But the ATPase in hepatic homogenate of ligation group were significantlyincreased and MPO,TNF-? and IL-6 in hepatic homogenate of ligation group were significantly lower as compared with non-ligation group.Conclusion The mechanism of mesenteric lymph duct ligation relieving hepatic injury of rats was related to the mesenteric lymph blockage reduces the TNF-? and IL-6 and improves the expression of BCL-2 protein and the activity of ATPase in liver.
