Effects of liver sinusoid endothelial cell injury in mouse hepatic veno-occlusive disease.
- Author:
Ting FANG
1
;
Li-Cai AN
;
Mi-Mi LIU
;
Jing HUA
;
Kai-Lin XU
;
Ling-Yu ZENG
Author Information
1. Department of Hematology, Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, Jiangsu Province, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Endothelial Cells;
pathology;
Endothelium;
cytology;
Hepatic Veins;
cytology;
pathology;
Hepatic Veno-Occlusive Disease;
chemically induced;
pathology;
Liver Cirrhosis;
chemically induced;
pathology;
Male;
Mice;
Mice, Inbred BALB C;
Monocrotaline;
adverse effects;
Platelet Adhesiveness
- From:
Journal of Experimental Hematology
2012;20(6):1457-1462
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to investigate the role of monocrotaline-inducing mouse liver sinusoid endothelial cell (SEC) injury in hepatic veno-occlusive disease. BALB/c mice were randomly divided into 2 groups: control group and monocrotaline group, mice were orally administrated with normal saline or monocrotaline with concentration of 200 mg/kg at days 0, 1, 2, respectively. At days 3, 4, 6, 8 and 10 after oral administration with normal saline or monocrotaline, the liver function (ALT, TBIL, AKP) and liver index were examined, and the percentage of activated platelets were detected by flow cytometry. The SEC, vascular endothelial cells and hepatic fibrosis were observed by staining with hematoxylin-eosin and Masson. Transmission electron microscopy was used to observe sinusoidal endothelial cell damage and platelet adhesion. The results showed that compared with control group, mice in monocrotaline group were characterized by severe damage of SEC, numbers of platelet aggregation and adhesion, central number and sinusoidal fibrosis. The percentage of activated platelets and liver index increased (P < 0.05). The characterization of portal hypertension was presented later, such as dysfunction of liver and ascites. It is concluded that SEC injury induced by monocrotaline may be the first step of hepatic veno-occlusive disease, and this kind of SEC injury is self-limiting, but fibrosis is always observed.
