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目的：观察茶多酚对肺癌小鼠移植瘤基质金属蛋白酶-2（MMP-2）及其相应的组织金属蛋白酶抑制剂-2（TIMP-2）表达的影响，探讨茶多酚抗新生血管生成的效应机制。方法：建立57 小鼠肺癌移植瘤模型，测定茶多酚低、高剂量组以及茶多酚联合沙利度胺组的肿瘤抑制率，并且采用免疫组化法检测各组MMP-2、TIMP-2 表达水平以及MMP-2/TIMP-2 比值，以探讨其抗肿瘤的分子机制。结果：实验表明，茶多酚有如下作用：①沙利度胺组、茶多酚低剂量组、茶多酚高剂量组、茶多酚低剂量联合沙利度胺组、茶多酚高剂量联合沙利度胺组的肿瘤抑制率分别为17.26 %、16.94 %、20.81 %、21.94 %和44.32 %，茶多酚高剂量联合沙利度胺组与模型组瘤重比较，有统计学意义（P＜0.05）；②茶多酚各组及联合用药各组能下调肿瘤组织MMP-2 蛋白表达，茶多酚高剂量联合沙利度胺组能上调TIMP-2 蛋白表达，与模型对照组比较，均具有统计学意义（P＜0.05）；③用药各组MMP-2/TIMP-2 比值均有所下降，茶多酚各组明显降低，茶多酚大剂量联合沙利度胺组比值下降最为显著。结论：茶多酚高剂量联合沙利度胺组对肺癌有明显抑制作用。其机制可能与下调MMP-2 表达、上调TIMP-2 表达、调整MMP-2/TIMP-2 比值失衡状态，从而抗肺癌新生血管生成相关。

英文摘要:

Objective: To observe the effect of Tea Polyphenols (TP) on the expression of matrix metalloproteinase-2 (MMP-2) and its corresponding tissue inhibitor of metalloproteinase-2 (TIMP-2) in Lewis lung cancer xenograft in mice, so as to explore TP's anti-angiogenesis mechanism. Methods: Lewis lung carcinoma was successfully implanted in 48 C57BL/6 mice, which were then randomly divided into six groups namely model control group, Thalidomide control group, TP low-dose group, TP high-dose group, TP low-dose combined with Thalidomide group and TP high dose combined with Thalidomide group. Tumor inhibition rates of these groups were examined, while MMP-2 and TIMP-2 expression was detected applying immunohistochemical technique and MMP-2/TIMP-2 ratio was calculated, in order to investigate the molecular mechanism of TP's anti-tumor effect. Results: According to our study, TP was proved to have the following effects: (1) The tumor inhibition rates of Thalidomide control group, TP low-dose group, TP high-dose group, TP low-dose plus Thalidomide group and TP high dose plus Thalidomide group were 17.26%, 16.94%, 20.81%, 21.94%, 44.32% respectively. Compared with model control group, the tumor inhibition rate rise in TP high dose plus Thalidomide group was of statistical difference (P<0.05). (2) Compared with model control group, the expression of MMP-2 was significantly down-regulated in all four groups containing TP (P<0.05), while TIMP-2 expression in TP high dose plus Thalidomide group was up-regulated (P<0.05). (3) The MMP-2/TIMP-2 ratio was reduced in every treatment group, and the ratio of TP high dose plus Thalidomide group was most obviously decreased. Conclusion: TP high dose plus Thalidomide can significantly inhibit Lewis lung cancer growth. And one of its possible mechanisms is to down-regulate MMP-2 expression, up-regulate TIMP-2 expression, reduce MMP-2/TIMP-2 ratio to normal range, thus play a important role in anti-angiogenesis process.

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