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The current study aimed to reveal a novel method for constructing a portal vein thrombosis (PVT) model in rats and to evaluate the inhibitory role of recombinant P-selectin glycoprotein ligand immunoglobulin G (rPSGL-Ig) on the formation of PVT. The PVT model was constructed in rats through intermittent portal vein obstruction (IPVO) combined with endangium destruction. A total of 4 mg/kg rPSGL-Ig was intraperitoneally pre-injected into rats 1 h prior to model construction. Changes in the thrombus size and vessel diameter were observed by B-scan ultrasonography. Histopathological changes in the portal vein, central hepatic vein and vasa intestini tenuis were observed using hematoxylin and eosin staining. Additionally, histopathological changes in the portal vein were observed by transmission electron microscopy. A total of 8 mg/kg rPSGL-Ig or 2×10 4 U/kg urokinase were used to compare the thrombolytic effects and thrombus sizes. The PVT model was successfully constructed in rats, and exhibited a significantly greater thrombus size and vessel diameter compared with the control group (P<0.05). Intervention with rPSGL-Ig significantly inhibited the formation of PVT, and resulted in a significantly lower thrombus size and vessel diameter compared with the model group (P<0.05). Additionally, histopathological changes in the portal vein, central hepatic vein and vasa intestini tenuis in PVT rats were considerably reversed following the intervention with rPSGL-Ig. rPSGL-Ig demonstrated a lower thrombolytic effect compared with that of URO. IPVO combined with endangium destruction effectively constructed a PVT model in rats. rPSGL-Ig effectively prevented PVT in rats. rPSGL-Ig may be used in future studies for the treatment of patients with PVT.
The current study aimed to reveal a novel method for constructing a portal vein thrombosis (PVT) model in rats and to evaluate the inhibitory role of recombinant P-selectin glycoprotein ligand immunoglobulin G (rPSGL-Ig) on the formation of PVT. The PVT model was constructed in rats through intermittent portal vein obstruction (IPVO) combined with endangium destruction. A total of 4 mg/kg rPSGL-Ig was intraperitoneally pre-injected into rats 1 h prior to model construction. Changes in the thrombus size and vessel diameter were observed by B-scan ultrasonography. Histopathological changes in the portal vein, central hepatic vein and vasa intestini tenuis were observed using hematoxylin and eosin staining. Additionally, histopathological changes in the portal vein were observed by transmission electron microscopy. A total of 8 mg/kg rPSGL-Ig or 2×10 4 U/kg urokinase were used to compare the thrombolytic effects and thrombus sizes. The PVT model was successfully constructed in rats, and exhibited a significantly greater thrombus size and vessel diameter compared with the control group (P<0.05). Intervention with rPSGL-Ig significantly inhibited the formation of PVT, and resulted in a significantly lower thrombus size and vessel diameter compared with the model group (P<0.05). Additionally, histopathological changes in the portal vein, central hepatic vein and vasa intestini tenuis in PVT rats were considerably reversed following the intervention with rPSGL-Ig. rPSGL-Ig demonstrated a lower thrombolytic effect compared with that of URO. IPVO combined with endangium destruction effectively constructed a PVT model in rats. rPSGL-Ig effectively prevented PVT in rats. rPSGL-Ig may be used in future studies for the treatment of patients with PVT.
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