茶多酚对小鼠Lewis肺癌移植瘤中NF-κB、COX-2、Survivin表达的影响

BACKGROUND AND OBJECTIVE: Lung cancer is the leading cause of cancer-related deaths worldwide. The anti-angiogenic effect of tea polyphenols (TPs) on lung carcinoma was confirmed in our previous study. The effect of TPs on the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), cyclooxygenase-2 (COX-2), and Survivin in Lewis lung cancer xenograft in mice was observed to explore the anti-angiogenic mechanism of TPs. METHODS: Lewis lung carcinoma was successfully implanted in 32 C57BL/6 mice, which were then randomly divided into the model control group, the Thalidomide group, the TPs group and the TPs combined with Thalidomide group. The tumor inhibition rates in these groups were determined, whereas the expressions of NF-κB, COX-2 and Survivin were detected using immunohistochemical techniques to investigate the molecular mechanism of the anti-tumor effect of TPs. RESULTS: (1) The tumor inhibition rates in the Thalidomide control group, the TPs group and the TPs plus Thalidomide group were 17.26%, 20.81%, 44.32% respectively. Compared with the model control group, the tumor inhibition rate was significantly higher in the TPs plus Thalidomide group (P < 0.05); (2) Compared with the model control group, the expression of NF-κB was significantly decreased in the TPs group and the TPs plus Thalidomide group, and it was significantly downregulated in the latter (P < 0.05); (3) The expression of COX-2 decreased in all treatment groups, and was significantly downregulated in the TPs plus Thalidomide group compared with the model control group (P < 0.05); (4) Compared with the model control group, Survivin expression was significantly downregulated in all treatment groups (P < 0.05), and was most obviously reduced in the TPs plus the Thalidomide group (P < 0.01). CONCLUSION: TPs plus Thalidomide significantly inhibits Lewis lung cancer growth. TPs possibly downregulates the expression of NF-κB, COX-2 and Survivin in tumor tissue, thereby playing important roles in anti-angiogenesis.