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Updated: May 25, 2026

Development and Angiographic Use of the Rabbit VX2 Model for Liver Cancer
Published on: January 7, 2019
Temperature-sensitive liquid embolic agent loaded with Lobaplatin in the TACE procedure for rabbit VX2 liver tumor
Yahua Li1, Junyao Chen1, Jialong Zhang1
1Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, No.1 Longhuzhonghuan Road, Zhengzhou, 450052, China.
Abstract:
To investigate the efficacy of a temperature-sensitive liquid embolic (TempSLE) agent loaded with lobaplatin for transarterial chemoembolization (TACE) in a rabbit VX₂ liver tumor model. Rabbit VX₂ liver tumor models were randomly divided into four groups: control, hepatic arterial infusion chemotherapy (HAIC), conventional TACE (C-TACE) with lipiodol, and experimental TACE (T-TACE) with TempSLE. Tumor volume, serum and intratumoral concentrations of lobaplatin (LBP), and serum levels of ALT, AST, and CREA were analyzed. Immunohistochemical (IHC) staining for PCNA, BCL-2, and HIF-1, as well as immunofluorescence (IF) staining for P53, cyclin B, and PD-L1, were evaluated. On postoperative day 7, tumor volumes were 5.17 ± 0.45 cm3 in the control group and 3.37 ± 0.22 cm3 in the HAIC group, which constituted a significant difference. No contrast enhancement was observed in the C-TACE and T-TACE groups, indicating complete tumor necrosis. On postoperative day 3, serum LBP concentration was significantly higher in the cTACE group than in the HAIC and T-TACE groups. By day 7, there were no intergroup differences in serum LBP. At both 3 and 7 days post-procedure, intratumoral LBP concentration was highest in the T-TACE group and lowest in the HAIC group. IHC and IF analyses revealed that T-TACE significantly down-regulated the expression of PCNA and BCL-2, but up-regulated HIF-1. Furthermore, T-TACE down-regulated cyclin B and P53 expression, while up-regulating PD-L1. This study demonstrates that TACE using TempSLE loaded with lobaplatin shows more favorable modulation of proliferation, apoptosis markers, and PD-L1 expression in tumor treatment.
