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目的 探讨环氧合酶 2 (COX 2 )在胰腺癌新生血管生成中的调节作用及其作用机制。方法 应用免疫组织化学染色研究人胰腺癌组织COX 2、血管内皮细胞生长因子 (VEGF)表达 ;同时标记肿瘤新生血管内皮细胞vWF和血管壁Ⅳ型胶原 ,计算肿瘤组织微血管密度 (MVD)。建立裸鼠胰腺癌细胞株PC 3移植瘤 ,观察选择性COX 2抑制剂Celebrex对肿瘤组织MVD的影响 ,并应用免疫组织化学染色和逆转录聚合酶链式反应 (RT PCR)研究裸鼠移植瘤组织VEGF表达变化。结果 COX 2在人胰腺癌组织中表达阳性率为 87 5 % ,VEGF阳性率为 5 8 3%。COX 2强阳性组MVD平均值显著高于COX 2弱阳性 +阴性组 ,P <0 0 1。VEGF阳性组MVD平均值高于VEGF阴性组 ,但无统计学差异 ,P >0 0 5 ;Pearson相关性检验结果表明COX 2与vWF和Ⅳ胶原标记的MVD均有明显的相关性 (相关系数分别为 0 5 99和 0 6 ) ,P <0 0 5。在裸鼠移植瘤的体内实验中 ,与对照组MVD(6 3 89± 13 6 7)相比 ,Celebrex处理组MVD为 32 2 5± 12 99,两者差异显著 ,P <0 0 1。免疫组织化学染色和RT PCR结果表明Celebrex处理组肿瘤组织VEGF表达较对照组明显下调。结论 COX 2与胰腺癌新生血管生成密切相关 ,其高表达促进了胰腺癌新生血管生成 ;可能作用机制是上调促血管生成因子VEGF
Objective To investigate the regulatory effect of cyclooxygenase 2 (COX 2) on neovascularization in pancreatic cancer and its mechanism. Methods Immunohistochemical staining was used to study the expression of COX-2 and VEGF in human pancreatic cancer. The vWF and the type Ⅳ collagen of vascular endothelial cells were also labeled to calculate the microvessel density (MVD) of tumor tissue. The effect of selective COX 2 inhibitor Celebrex on MVD of pancreatic cancer cell line PC 3 was observed. Immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) Tissue VEGF expression changes. Results The positive rate of COX 2 in human pancreatic cancer was 87.5% and the positive rate of VEGF was 58.3%. The average MVD in COX 2 strongly positive group was significantly higher than that in COX 2 weak positive + negative group, P <0.01. The mean MVD of VEGF-positive group was higher than that of VEGF-negative group, but there was no significant difference (P> 0.05). Pearson correlation test showed that COX 2 was significantly correlated with vWF and Ⅳ collagen-labeled MVD 0 5 99 and 0 6), P <0 0 5. In in vivo experiments in nude mice, the MVD of Celebrex-treated group was 32 2 5 ± 12 99 compared to MVD of control group (6 3 89 ± 13 6 7), with significant difference between the two groups (P <0.01). Immunohistochemical staining and RT PCR results showed that the expression of VEGF in the tumor tissue of Celebrex treatment group was significantly lower than that in the control group. Conclusions COX 2 is closely related to angiogenesis of pancreatic cancer. High expression of COX 2 promotes angiogenesis of pancreatic cancer. The possible mechanism is upregulation of pro-angiogenic factor VEGF