Abstract

Effects of NF-kB and the role of inflammatory response factors on the hepatocytic injury after TAE- An experimental study

Author(s): Bimbadhar Valluru, Wang Bei Ran, Du Wei, Yu Yi Jun,Wu Chun Hua & Kalyan Sharma

Objective: To investigate the effects of NF-κB and the role of inflammatory response factors on the normal liver tissue around the tumors in rabbit VX2 hepatocellular carcinoma models after TAE. Methods: Seventy VX2 hepatoma rabbit models were prepared and success rate was 85.7%. Computed tomography (CT) and Magnetic resonance imaging (MRI) was performed after 21 days of modelling. Sixty rabbits were randomly chosen and divided into three groups, 20 in each group: TAE group, Contrast/Angiography group, and Control group respectively. TAE group was treated with Transarterial embolization (TAE) and the Contrast group was subjected to hepatic arteriography and DSA, while the Control group served as a control group. The immune-histochemistry analysis was used to detect the expression of NF-κB in normal liver tissue around the tumors of each group. The levels of inflammatory factors like TNF-α, IL-10 of each group were detected by Enzyme-linked immunosorbent assay (ELISA) in the normal liver tissue around the tumor. Using SPSS 22.0 statistical analysis software, measurement data was analyzed using t-test, count data were compared using the χ2-test; P <0.05 was considered as statistically significant. Results: The positive expression rates of NF-κB in the TAE group, contrast group, and control group were 75% (15/20), 35% (7/20) and 20% (4/20) respectively. The concentrations of TNF-α were 11.72 ± 0.65 (ng/L), 9.60 ± 0.31 (ng/L) and 8.82 ± 0.81 (ng/L); the concentrations of IL-10 were 2.18±0.13 (ng/L), 1.67 ± 0.12 (ng/L), 1.66 ± 0.10 (ng/L) respectively. Compared with the control group and contrast groups, TAE group showed a significant increase in the expression of NF-κB, and the levels of TNF-α and IL-10 were also increased. Conclusion: The hepatocytic injury, degrading function after TAE could be due to the interaction of NF-κB and inflammatory factors- TNF-α and IL-10.


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