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目的研究重组血管内皮抑素(ES)对荷人食管鳞癌裸鼠血管内皮生长因子-C(VEGF-C)和淋巴管内皮细胞透明质酸受体-1(LYVE-1)的调节作用。方法构建人食管鳞癌裸鼠模型,6只瘤周皮下注射ES稀释液荷瘤裸鼠作为A组,6只瘤周皮下注射生理盐水荷瘤裸鼠作为B组,6只正常裸鼠作为C组,比较三组血清LYVE-1、VEGF-C的表达水平,观察ES对荷瘤裸鼠LYVE-1和VEGF-C基因表达的影响。结果 A、B组血清VEGF-C水平分别为(155.26±10.24)、(180.23±15.64)pg/L,均高于C组的(103.15±13.20)pg/L,差异具有统计学意义(P<0.01);A组血清VEGF-C水平低于B组,差异具有统计学意义(P<0.05)。A、B组血清LYVE-1水平分别为(65.32±16.29)、(90.58±10.67)pg/L,均高于C组的(28.31±10.36)pg/L,差异具有统计学意义(P<0.01);A组血清LYVE-1水平低于B组,差异具有统计学意义(P<0.05)。A、B组组织内VEGF-C、LYVE-1的PCR扩增倍数均高于C组,差异具有统计学意义(P<0.01);A组组织内VEGF-C、LYVE-1的PCR扩增倍数低于B组,差异具有统计学意义(P<0.05)。结论通过重组ES对TE-1食管鳞癌细胞荷瘤裸鼠干预,重组ES不仅抑制肿瘤新生血管的生成,而且重组ES可能通过抑制肿瘤组织内VEGF-C和LYVE-1的表达,对肿瘤新生淋巴管的发生起到抑制作用。
Objective To investigate the regulatory effect of recombinant endostatin (ES) on vascular endothelial growth factor-C (VEGF-C) and lymphatic endothelial cell hyaluronan receptor-1 (LYVE-1) in human esophageal squamous cell carcinoma. Methods The human esophageal squamous cell carcinoma model was constructed in nude mice. Six tumor-bearing nude mice were injected subcutaneously with ES diluted tumor-bearing nude mice as group A. Six nude mice were injected subcutaneously with normal saline as tumor bearing nude mice as group B and six normal nude mice as group C Group. The expression of LYVE-1 and VEGF-C in the three groups were compared, and the effect of ES on LYVE-1 and VEGF-C gene expression in nude mice was observed. Results The serum levels of VEGF-C in group A and group B were (155.26 ± 10.24) and (180.23 ± 15.64) pg / L, respectively, which were significantly higher than those in group C (103.15 ± 13.20) pg / L, 0.01). The serum level of VEGF-C in group A was lower than that in group B, the difference was statistically significant (P <0.05). The levels of serum LYVE-1 in group A and group B were (65.32 ± 16.29) and (90.58 ± 10.67) pg / L, respectively, which were significantly higher than those in group C (28.31 ± 10.36) pg / L ); The level of serum LYVE-1 in group A was lower than that in group B, the difference was statistically significant (P <0.05). The PCR amplification of VEGF-C and LYVE-1 in group A and group B were all higher than that in group C (P <0.01). The PCR amplification of VEGF-C and LYVE-1 in group A The multiple was lower than that in group B, the difference was statistically significant (P <0.05). Conclusion Recombinant ES can not only inhibit tumor angiogenesis but also inhibit the expression of VEGF-C and LYVE-1 in tumor tissue through recombinant ES intervention on TE-1 esophageal squamous cell carcinoma in nude mice. Lymphangiogenesis plays a suppressive role.