ABSTRACT
To investigate the effect of schisantherin A on liver sinusoid endothelial cell function and angiogenesis. Different dosages (0-40 μmol•L⁻¹) of schisantherin A were incubated 24 h with SK-HEP-1 cells, and the toxicity of SK-HEP-1 cells was assayed by MTT method. The proliferation of SK-HEP-1 cells were induced by the vascular endothelial growth factor (VEGF), with receptor tyrosine kinase inhibitor sorafenib as the control, at the same time, set up the control group, 2, 20 μmol•L⁻¹ schisantherin A were incubated with SK-HEP-1 cells, cell proliferation was analyzed by EdU DNA cell proliferation kit. Fluorescence probe method was used to assay the intracellular NO levels and NOS activity. Tube formation was observed using cell migration and a matrigel tube formation assay. Rat aortic ring assay was performed to observe the sprouting vessels from aortic ring. The fluorescence vessels, the number of functional blood vessels, and intersegmental vessel changes of transgenic zebrafish were also observed. Compared with control group, the proliferation of SK-HEP-1 cells induced by VEGF increased and and the level of NO and NOS activity induced; compared with model group, 2, 20 μmol•L⁻¹ schisantherin A and sorafenib inhibited the proliferation of SK-Hep-1 cells induced by VEGF, and reduced the level of NO and NOS activity. At the dosage of 20 μmol•L⁻¹, schisantherin A attenuated the migration and tube formation of SK-HEP-1 cells induced by VEGF, and also inhibition the formation of rat aortic rings and intersegmental vessel changes of transgenic zebrafish, and significantly reduce the number of vessels in zebrafish. Schisantherin A has potential effects on function of endothelial cell proliferation and angiogenesis.
ABSTRACT
Objective To explore the relationship between CD34 expression or microvessel density and hepatic fibrosis degree in advanced schistosomiasis patients.MethodsThirty-five advanced schistosomiasis patients and 5 control patients were included in this study.CD34 expression in liver tissue was measured with immunohistochemistry while microvessel density(MVD)of liver tissue was evaluated under a light microscope.ResultsCD34 expression and MVD value were significantly correlated with hepatic fibrosis degree in liver tissue from the advanced schistosomiasis patients.ConclusionsCD34 expression and MVD value are two histological parameters representing the liver sinusoid changes during fibrogenesis in advanced schistosomiasis patients.
ABSTRACT
Objective To observe the change of liver sinusoid in BALB/c mice infected with Schistosoma japonicum and explore its relationship between the degree of hepatic fibrosis and liver function. Methods A model was established in BALB/c mice infected with cercariae of Schistosoma japonicum. The liver specimens of mice were used for pathological examination with routine and picric acid-sirius red staining to know the degree of hepatic fibrosis by semi-quantity. The expressions of C-IV and vWF in liver sinusoid were assayed through the immuhistochemistry staining. The serum ALT and AST were detected by the automatic biochemistry analyzer, and the ultramicrostructure of the liver tissue was observed by a transmission electron microscope. Results The number and diameter of fenestrations in SEC reduced 4 weeks after the infection. The fenestrations were disappeared and the base membrane established 8 weeks after the infection. The expressions of C-IV and vWF in liver sinusoid and the degree of hepatic fibrosis increased with the time after infection. The levels of serum ALT and AST were not correlated with the infection time. Conclusions The phenotype alteration of the hepatic sinusoidal endothelium may be a vital issue triggering the liver fibrosis induced by Schistosoma japoncium.