【摘要】 目的通过检测非小细胞肺癌(NSCLC)中核转录因子κb p65(NF-κB p65)蛋白、CD68阳性细胞的表达,探讨它们在肺癌发生发展中的作用以及两者的关系。方法免疫组化SP法检测67例人NSCLC标本(每个标本取癌组织、癌旁组织、正常组织)中NF-κB p65和CD68的表达,多组间比较运用单因素方差分析,并采用Pearson相关分析NF-κB p65蛋白表达与CD68阳性细胞数量的相关性。结果肺癌组织、癌旁组织、正常组织中NF-κB p65的平均光密度值分别为0.174±0.034,0.139±0.016,0.090±0.01;CD68阳性细胞数分别为11.779±1.368,97.486±2.538,52.140±1.853,组间比较差异均有统计学意义(P﹤0.05)。CD68的表达与TNM分期、淋巴节转移、是否侵及胸膜有关(P﹤0.05)。NF-κB p65蛋白在NSCLC中的表达与癌组织分化程度、TNM分期、淋巴节转移及是否侵及胸膜有关(P﹤0.05)。CD68阳性细胞数量和NF-κB p65蛋白的表达呈正相关(r=0.416,P﹤0.05)。结论 NF-κB p65蛋白的表达和CD68+巨噬细胞的浸润与NSCLC的发生发展转移相关,提示CD68+巨噬细胞可能通过激活NF-κB促进非小细胞肺癌的发生发展。更多还原

【Abstract】 OBJECTIVE To study the expression of NF-κB p65 protein and CD68 in non-small cell lung cancer(NSCLC),and their relationship with the development of lung cancer.METHODS Immunohistochemical SP method was used to analysed the expression of NF-κB p65 protein and CD68 in 67 cases of NSCLC samples including cancer tissues,adjacent tissues and normal tissues,and the statistical significances among groups were detected by One-Way ANOVA(SNK)and the relativity of CD68+ cell number with the expression of NF-κB p65 protein was investigated by Pearson correlation analysis.RESULTS The mean optical density of NF-κB p65 protein in cancer tissues,adjacent tissues and normal tissues was 0.174 ± 0.034,0.139 ± 0.016,0.090 ± 0.01;CD68+ cell number in cancer tissues,adjacent tissues and normal tissues was 11.779 ± 1.368,97.486 ± 2.538,52.140 ± 1.853,and there were statistical significance between groups(P﹤0.05).The expression of CD68 was correlative with the TNM grade,lymph nodes metastases and involvement of pleura(P﹤0.05).The expression of NF-κB p65 protein was consistent with the case of CD68 except that it was correlative with the differentiation of lung cancer(P﹤0.05).There was a positive correlation between the expression of NF-κB p65 protein and CD68+ cell counts(r = 0.416,P﹤0.05).CONCLUSION CD68+ macrophage infiltration and NF-κB p65 protein expression are relative with the development and metastasis of tumor,suggesting that CD68+ macrophage may be promote non-small cell lung cancer by activating NF-κB.更多还原