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目的探讨环氧化酶-2(COX-2)对非小细胞肺癌(NSCLC)血管内皮生长因子(VEGF)的表达及血管生成的影响。方法应用免疫组化技术检测NSCLC中COX-2、VEGF的表达和微血管密度(MVD),采用噻唑蓝(MTT)法观察阿司匹林对肺腺癌A549细胞增殖的影响,采用免疫细胞化学法观察阿司匹林对A549细胞VEGF表达的影响。结果(1)COX-2在NSCLC组织中的阳性表达率为62.5%,COX-2表达与VEGF表达显著相关(r=0.62,P<0.05),COX-2阳性组MVD(49.55±17.18)高于COX-2阴性组(34.65±22.25),COX-2和VEGF均阳性组MVD(51.71±15.42)明显高于两者均阴性组(28.70±18.94),差异均有高度统计学意义(均P<0.01)。(2)阿司匹林呈剂量依赖方式抑制A549细胞增殖,48h细胞最大抑制率达65.49%,10mmol/L阿司匹林作用A549细胞48h后,A549细胞VEGF表达明显降低(作用前后分别为0.109±0.012与0.517±0.034),差异有高度统计学意义(P<0.01)。结论NSCLC组织中存在COX-2的高表达,其通过增加VEGF表达促进肺癌血管的形成,进而促进肺癌的进展;阿司匹林可抑制A549细胞增殖,其作用可能与下调COX-2和VEGF的表达有关。
Objective To investigate the effect of cyclooxygenase-2 (COX-2) on the expression of vascular endothelial growth factor (VEGF) and angiogenesis in non-small cell lung cancer (NSCLC). Methods The expression of COX-2, VEGF and microvessel density (MVD) in NSCLC were detected by immunohistochemistry. The effects of aspirin on the proliferation of lung adenocarcinoma A549 cells were observed by MTT assay. The immunostaining of aspirin Effect of VEGF expression in A549 cells. Results (1) The positive expression rate of COX-2 in NSCLC was 62.5%, the expression of COX-2 was significantly correlated with the expression of VEGF (r = 0.62, P <0.05) The MVD (51.71 ± 15.42) in COX-2 negative group (34.65 ± 22.25), COX-2 and VEGF positive group were significantly higher than those in both negative group (28.70 ± 18.94), the differences were statistically significant (P <0.01). (2) Aspirin inhibited the proliferation of A549 cells in a dose-dependent manner, the maximum inhibitory rate was 65.49% at 48h, and the A549 cells treated with 10mmol / L aspirin 48h significantly decreased the expression of VEGF (A549 cells before and after 0.109 ± 0.012 and 0.517 ± 0.034 ), The difference was highly statistically significant (P <0.01). Conclusion The high expression of COX-2 in NSCLC tissues may promote the formation of lung cancer by increasing the expression of VEGF, which may further promote the progression of lung cancer. Aspirin can inhibit the proliferation of A549 cells, which may be related to the down-regulation of the expression of COX-2 and VEGF.