BACKGROUND:The active form of nuclear factor-kappa B(NF- κB)is involved in the initiation,generation,and development of hepatocellular carcinoma(HCC),and is up-regulated in inflammation-associated malignancies.We investigated the dynamic expression of NF-κB and its influences on the occurrence of HCC through antiangiogenic(thalidomide) intervention in NF-κB activation. METHODS:Hepatoma models were induced with 2-fluorenyl- acetamide(2-FAA,0.05%)in male Sprague-Dawley rats,and thalidomide(100 mg/kg body weight)was administered intragastrically to intervene in NF-κB activation.The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining.NF-κB mRNA was amplified by RT-nested PCR.The alterations of NF-κB and vascular endothelial growth factor(VEGF)expression were analyzed by enzyme-linked immunosorbent assay,immunohistochemistry,and Western blotting. RESULTS:Rat hepatocytes showed denatured,precancerous,and cancerous stages in hepatocarcinogenesis,with an increasing tendency of hepatic NF-κB,NF-κB mRNA,and VEGF expression,and their values in the HCC group were higher than those in controls(P<0.001).In the thalidomide- treated group,the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages,and nodular hyperplasia or a little atypical hyperplasia at the final stages,with the expression of NF-κB (χ2=9.93,P<0.001)and VEGF(χ2=8.024,P<0.001)lower than that in the 2-FAA group. CONCLUSION:NF-κB is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-κB and VEGF,and delays the occurrence of HCC. BACKGROUND: The active form of nuclear factor-kappa B (NF- κB) is involved in the initiation, generation, and development of hepatocellular carcinoma (HCC), and is up-regulated in inflammation-associated malignancies. We investigated the dynamic expression of METHODS: Hepatoma models were induced with 2-fluorenyl-acetamide (2-FAA, 0.05%) in male Sprague-Dawley rats, and thalidomide (100 mg / kg body weight) were administered intragastrically to intervene in NF-κB activation. Pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining. NF-κB mRNA was amplified by RT-nested PCR. The alterations of NF-κB and vascular endothelial growth factor (VEGF) expression were analyzed by enzyme-linked immunosorbent assay, immunohistochemistry, and Western blotting. RESULTS: Rat hepatocytes showed denatured, precancerous, and cancerous stages in hepatocarc inogenesis, with an increasing tendency of hepatic NF-κB, NF-κB mRNA, and VEGF expression, and their values ​​in the HCC group were higher than those in controls (P <0.001). The thalidomide-treated group, the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages, and nodular hyperplasia or a little atypical hyperplasia at the final stages with the expression of NF-κB (χ2 = 9.93, P <0.001) and VEGF (χ2 = 8.024, P <0.001) lower than that in the 2-FAA group. CONCLUSION: NF-κB is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-κB and VEGF, and delays the occurrence of HCC.