Cultured mycelium Cordyceps sinensis (CMCS) was widely used for a variety of diseases including liver injury, the current study aims to investigate the protective effects of CMCS on liver sinusoidal endothelial cells (LSECs) in acute injury liver and related action mechanisms. The mice were injected intraperitoneally with
lipopolysaccharide (LPS) and D-
galactosamine (D-GalN). 39 male BABL/c mice were randomly divided into four groups: normal control, model control, CMCS treatment and
1,10-phenanthroline treatment groups. The Serum liver function parameters including
alanine aminotransferase (ALT) and
aspartate aminotransferase (AST) levels were assayed with the commercial kit. The
inflammation and scaffold structure in liver were stained with
hematoxylin and
eosin and
silver staining respectively. The LSECs and sub-endothelial basement membrane were observed with the scanning and transmission electronic microscope. The
protein expressions of
intercellular adhesion molecule-1 (ICAM-1) and
vascular cell adhesion molecule-1 (VCAM-1) in liver were analyzed with Western blotting. Expression of
von Willebrand factor (vWF) was investigated with immunofluorescence staining. The lipid peroxidation indicators including antisuperoxideanion (ASAFR),
hydroxyl free radical (·OH),
superoxide dismutase (SOD),
malondialdehyde and
glutathione S-transferase (GST) were determined with kits, and
matrix metalloproteinase-2 and 9 (
MMP-2/9) activities in liver were analyzed with
gelatin zymography and in situ fluorescent zymography respectively. The model mice had much higher serum levels of ALT and AST than the normal mice. Compared to that in the normal control, more severe liver
inflammation and hepatocyte apoptosis, worse hepatic lipid peroxidation demonstrated by the increased ASAFR, ·OH and MDA, but decreased SOD and GST, increased
MMP-2/9 activities and
VCAM-1,
ICAM-1 and vWF expressions, which revealed obvious LSEC injury and scaffold structure broken, were shown in the model control. Compared with the model group, CMCS and
1,10-phenanthroline significantly improved serum ALT/AST, attenuated hepatic
inflammation and improved peroxidative injury in liver, decreased
MMP-2/9 activities in liver tissue, improved integration of scaffold structure, and decreased
protein expression of
VCAM-1 and
ICAM-1. CMCS could protect LSECs from injury and maintain the microvasculature integration in acute injured liver of mice induced by LPS/D-GalN. Its action mechanism was associated with the down-regulation of
MMP-2/9 activities and inhibition of peroxidation in injured liver.