中文摘要：

目的观察体外培养的肿瘤细胞对巨噬细胞炎症因子--肿瘤坏死因子-α（TNF-α）的诱导作用；初步探索羧胺三唑（CAI）对肿瘤诱导的巨噬细胞中 TNF-α释放的影响。方法利用 transwell 装置，建立 Lewis 肺癌细胞（LLC）与 RAW264.7巨噬细胞共培养体系，采用荧光定量 PCR方法和 ELISA 方法分别分析 RAW264.7中 TNF-α的表达和释放；用 LLC 条件培养基（LCM）诱导 RAW264.7，同时给予 CAI 处理，采用 CCK-8方法分析 LCM 和 CAI对 RAW264.7活力的影响，采用 ELISA 方法分析 CAI 对诱导后的 RAW264.7中 TNF-α释放的影响。 结果与 LLC 共培养24 h 可显著增加 RAW264.7中TNF-α相对表达量[单独培养 vs 共培养，（1.00±0.12）vs （2.23±0.17），P 〈0.01]和释放[单独培养 vs 共培养，（65.21±12.76）vs （143.92±19.22）pg/ml，P〈0.05]；LCM 和 CAI 在1 h 和4 h 对 RAW264.7活力没有影响，CAI 可以显著抑制 LCM 对 RAW264.7中 TNF-α释放的诱导（4 h，P〈0.01）。 结论 LLC 肿瘤微环境可以诱导 RAW264.7中 TNF-α的表达增加；CAI 对这种诱导的抑制使其在肿瘤环境中表现出一定的抗炎作用，可能是其抗肿瘤作用的机制之一。

英文摘要：

Objective To investigate the tumor necrosis factor-α（TNF-α） expression and secretion enhancement in macrophages induced by tumor cells in vitro, as well as the inhibitory effect of carboxyamidotriazole （CAI） on TNF-α induction in tumor-educated macrophages. Methods The Lewis lung carcinoma （LLC） cells and RAW264.7 macrophages were co-cultured with the transwell inserts, LLC conditioned medium （LCM） was also used to induce RAW264.7 with or without CAI treatment. Real time RT-PCR and ELISA methods were applied to analyze the TNF-αexpression and secretion in RAW264.7, respectively. CCK-8 was applied to determine the effect of LLC （LCM） and CAI on the viability of RAW264.7. Results TNF-αexpression [cultured alone vs co-cultured, （1.00 ± 0.12） vs （2.23 ± 0.17）, P〈0.01] and secretion [cultured alone vs co-cultured, （65.21 ± 12.76） vs （143.92 ± 19.22） pg/ml, P〈0.05] were greatly increased in RAW264.7 after being co-cultured with LLC for 24 hours. LCM and CAI did not influence the viability of RAW264.7 at 1 hour and 4 hour, while CAI inhibited TNF-αsecretion in RAW264.7 induced by LCM （4 h, P〈0.01）. Conclusion LLC tumor environment can greatly enhance the TNF-α expression in RAW264.7. CAI inhibits this induction significantly and shows anti-inflammation activity in tumor environment, which may contribute to its anti-cancer effects.