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以小鼠Lewis肺癌(Lewis lung carcinoma,LLC)自发转移和小鼠黑色素瘤(B16)细胞实验转移为模型,检测福安泰-03(Fuantai-03,FAT-03)对小鼠Lewis肺癌生长和转移的影响,Western印迹和免疫组化法分析FAT-03对小鼠Lewis肺癌转移相关基因CD44和nm23-H1表达水平的影响。结果显示,FAT-03明显抑制LLC的生长和肝转移,显著抑制B16细胞的肺转移,并与环磷酰胺(CY)有协同作用。每天腹腔注射FAT-03 10.0、20.0 mg/kg,共用药14天,对LLC生长的抑制率分别为53.8%、61.3%(CY的抑制率为58.8%);对LLC肝转移的抑制率分别为37.4%、76.5%(CY的抑制率为64.5%)。对B16细胞肺转移的抑制率分别为51.4%和63.7%(CY的抑制率为44.0%,10.0mg/kg FAT-03+CY的抑制率为88.1%)。显著下调促癌转移基因CD44,上调抑癌转移基因nm23-H1的表达。结果提示FAT-03值得作为一种具有抗癌转移作用的先导物质继续研究,它的抗癌转移效果可能部分与其下调促癌转移基因CD44和上调抑癌转移基因nm23-H1的表达有关。
To investigate the effects of Fuantai-03 (FAT-03) on the growth and metastasis of Lewis lung carcinoma in mice with spontaneous metastasis of Lewis lung carcinoma (LLC) and experimental metastasis of mouse melanoma (B16) The effect of FAT-03 on the expression of CD44 and nm23-H1 in Lewis lung carcinoma in mice was analyzed by Western blot and immunohistochemistry. The results showed that FAT-03 significantly inhibited the growth and liver metastasis of LLC, significantly inhibited the lung metastasis of B16 cells and synergized with cyclophosphamide (CY). The intra-peritoneal injection of FAT-03 10.0,20.0 mg / kg for 14 days, the inhibition rate of LLC growth were 53.8%, 61.3% (CY inhibition rate of 58.8%); the inhibition rate of LLC liver metastasis were 37.4%, 76.5% (CY inhibition rate was 64.5%). The inhibition rates on lung metastasis of B16 cells were 51.4% and 63.7% respectively (the inhibition rate of CY was 44.0% and the inhibition rate of 10.0 mg / kg FAT-03 + CY was 88.1%). Significantly downregulation of cancer metastasis gene CD44, up-regulation of tumor suppressor gene nm23-H1 expression. The results suggest that FAT-03 is worth further research as a lead substance with anti-cancer metastasis effect, and its anti-cancer metastasis effect may be partly related to its down-regulation of CD44 and up-regulation of tumor suppressor gene nm23-H1.