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.