中文摘要：

肿瘤与炎症密切相关，作者以往已证实内源性促炎症缓解介质脂氧素A4（Lipoxin A4，LXA4）能在整体和细胞水平发挥抗肝癌细胞增殖和转移的作用。为进一步探讨LⅪ钆通过调节肿瘤相关巨噬细胞对肝癌细胞株HepG2microRNAs（miRNAs）表达谱的影响，该文首先提取经脂多糖（LPS）或LPS＋LXA4作用24h的人巨噬细胞株U937培养上清液，分别称为ACM或LCM，以模拟肿瘤的炎症微环境，并用此上清液刺激HepG2细胞，24h后提取细胞总RNA，采用microRNA芯片miRCURY^TM LNA Array（V16．0）检测，计算各样本中的miRNAs标准值及比值。以两组间Hy3荧光标记信号强度的比值≤0．5或≥2为标准判定差异表达miRNA。Real-time PCR检测Nhsa-miR-623的相对含量以验证基因芯片的结果。结果发现，与对照组细胞相比，经过ACM作用24h的HepG2细胞有35个miRNAs上调、130个miRNAs下调。LCM组与ACM组相比，HepG2细胞有185个miRNAs上调、71个miRNAs下调。Real-time PCR检测的结果证实，hsa-miR-623的变化与基因芯片趋势一致。综上所述，LXA4能通过肿瘤相关巨噬细胞而间接发挥其调节HepG2细胞miRNAs表达谱的作用。

英文摘要：

On the basis that the pathologic process of tumor is closely related to uncontrolled inflammation, we have proved that Lipoxin A4 （LXA4） could inhibit the proliferation and metastasis of HCC cells both in vitro and in vivo. This study further investigated the indirect effect of Lipoxin A4 （LXA4） on the microRNA （miRNA） expression profile in HepG2 cells through modulating the tumor-associated macrophages. Conditioned cell culture media from LPS-stimulated and LPS/LXA4 co-stimulated U937 cells, as ACM and LCM respectively, were collected. HepG2 cells were separated into control group, ACM group and LCM group, which were cultured in normal culture media, ACM and LCM for 24 hours, respectively, miRNAs were extracted and hybridized to miR-CURYTM LNA Array （V16.0）. It was considered to be up- or down- regulated when the miRNAs fluorescent intensity ration be- tween two groups was over 2 or less than 0.5. Validation of microarray results was carried out by Real-time PCR of hsa-miR-623. Compared with control group, ACM treatment for 24 h up-regulated 35 miRNAs and down-regulated 130 miRNAs in HepG2 cells, while LCM group had 185 miRNAs higher and 71 miRNAs lower than ACM group. Hsa-miR-623 showed similar variation with microarray. Our study indicated that LXA4 could indirectly regulate the miRNAs expression profile in HepG2 cells through modulating the tumor-associated macrophages.