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目的研究长链非编码RNA(lnc RNA)肺腺癌转移相关转录本1(MALAT1)对巨噬细胞极化的影响。方法采用佛波酯诱导人THP-1细胞分化为成熟的巨噬细胞,IFN-γ/LPS刺激诱导M1型极化,IL-4刺激诱导M2型极化,采用实时荧光定量PCR(RT-q PCR)检测各组细胞中MALAT1的表达。si RNA干扰巨噬细胞MALAT1表达,加入IL-4继续诱导M2型极化,RT-q PCR检测极化相关基因表达;酶联免疫吸附试验(ELISA)检测TNF-α、IL-12、CCL22、IL-10的水平。si RNA干扰M2型巨噬细胞MALAT1表达,研究其对M2极化表型的影响。结果 MALAT1在M2型巨噬细胞中表达显著升高,M1向M2极化改变MALAT1表达升高,而M2向M1极化改变MALAT1表达降低。MALAT1干扰后,IL-4诱导的M2型巨噬细胞TNF-α、IL-12分泌升高,CCL22、IL-10分泌降低;CXCL10、CXCL11、HLA-DR表达升高,CCL17、CCL18、CD163表达降低。M2型巨噬细胞MALAT1干扰后,TNF-α、IL-12分泌升高,CCL22、IL-10分泌降低。结论 MALAT1参与调控巨噬细胞极化,干扰MALAT1表达有效抑制M2型巨噬细胞极化,促进M1型巨噬细胞极化。
Objective To investigate the effect of long chain noncoding RNA (lnc RNA) metastasis associated lung cancer 1 transcript 1 (MALAT1) on macrophage polarization. Methods Phosphatidylinositol induced differentiation of human THP-1 cells into mature macrophages. M1-type polarization was induced by IFN-γ / LPS stimulation and M2-type polarization by IL-4 stimulation. Real-time fluorescence quantitative PCR PCR) to detect the expression of MALAT1 in each group of cells. The expression of MALAT1 in macrophages was stimulated by si RNA, and M2-type polarization was induced by addition of IL-4, and the expression of polarization-related genes was detected by RT-q PCR. The expressions of TNF-α, IL-12 and CCL22 were detected by enzyme linked immunosorbent assay (ELISA) IL-10 levels. si RNA interfered with MALAT1 expression in M2 macrophages to investigate its effect on M2 polarization phenotype. Results The expression of MALAT1 in M2 macrophages was significantly increased. The expression of MALAT1 was increased in M1 and M2, while MALAT1 was decreased in M2 and M1. After MALAT1 interference, the secretion of TNF-α and IL-12 of M2 macrophages induced by IL-4 increased and the secretion of CCL22 and IL-10 decreased; the expression of CXCL10, CXCL11 and HLA-DR increased, the expressions of CCL17, CCL18 and CD163 reduce. M2 macrophage MALAT1 interference, TNF-α, IL-12 secretion, CCL22, IL-10 secretion decreased. Conclusions MALAT1 is involved in the regulation of macrophage polarization and interference with MALAT1 expression, which can effectively inhibit the polarization of M2 macrophages and promote the polarization of M1 macrophages.