Effect Of Hepatocyte Growth Factor On The Organization And Recanalization Of Portal Vein Thrombosis Through JAK2-STAT3 Signaling Pathway

Objective: To establish a portal vein thrombosis(PVT)model to investigate the effect and mechanism of hepatocyte growth factor(HGF)on intravascular revascularization and thrombosis organization and recanalization in portal vein thrombosis after hepatic cell growth factor adenovirus heavy vector(ad-HGF)is injected into local portal vein thrombosis.Methods: 1.The portal vein thrombosis model is established.The 24 dogs with successful portal vein thrombosis model are randomly divided into three groups: control group,anticoagulation group and experimental group,and there are 8 dogs in each group.The experimental group is injected with ad-HGF and subcutaneous injection of low molecular weight heparin sodium.The anticoagulation group is injected into the same volume of normal saline and has a hypodermic needle of low molecular weight heparin sodium with experimental group,and the control group is injected into same volume of saline with that of the experimental group.2.After routine feeding for 7 days,the thrombus segmental portal vein is taken,HE staining is used to observe angiogenesis,organization and recanalization,and vWF immunohistochemical staining is used to observe the same site HGF and p-JAK2 expression;3.real-time quantitative PCR is used to detect the expression of HGF and VEGF mRNA.Western blot is used to detect the expression of HGF and signing pathway p-JAK2,p-STAT3 and VEGF protein.Results: 1.The model of portal vein thrombosis is successfully established.2.HE staining shows that the number of angiogenesis in the experimental group is higher than that in the control group and anticoagulation group.The immunohistochemical staining of vWF indicates that the phosphorylation of JAK2 protein is positively correlated with the high expression of HGF.3.Real-time quantitative PCR detection shows that the expression of HGF mRNA in the experimental group is significantly higher than that in the control group and the anticoagulation group.The expression of VEGF mRNA is higher in the experimental treatment group than in the anticoagulation group,and its expression in the anticoagulation group is higher than in the control group(P < 0.05).The difference is statistically significant;Western blot protein detection shows that the expression of HGF protein in the experimental group is significantly higher than that in the control group and the anticoagulation group(P <0.05);the expression of p-JAK2,p-STAT3 and VEGF protein in the experimental group is higher than that in the anticoagulation group.Its expression in the anticoagulant group is higher than in the control group(P <0.05),and the difference is statistically significant.Conclusion: 1.HGF can promote angiogenesis in portal vein thrombosis to accelerate the organization and recanalization of thrombus.2.That Ad-HGF promotes the organization and recanalization of portal vein thrombosis is related to the activation of the signaling pathway JAK2/STAT3.