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目的 探讨阿奇霉素在脂多糖(Lipopolysaccharide,LPS)刺激下对人单核白血病细胞THP-1髓系细胞触发受体-1(Triggering receptor expressed on myeloid cells-1,TREM-1)的调节作用及TREM-1调控对炎症反应的意义。方法将THP-1细胞分为LPS组(加入1μg/ml LPS)、LPS+TREM-1/FC融合蛋白组(加入1μg/ml LPS和1μg/ml TREM-1/FC融合蛋白)和LPS+阿奇霉素组(加入1μg/ml LPS和10μg/ml阿奇霉素)。分别于培养4、8、12、24、48 h后,采用RT-PCR和Western blot法检测各组细胞中TREM-1基因mRNA及蛋白的表达,ELISA法检测各组细胞上清液中可溶性TREM-1(Soluble TREM-1,sTREM-1)、肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)、白细胞介素-6(Interleukin-6,IL-6)和白细胞介素-1β(Interleukin-1β,IL-1β)的水平。结果 TREM-1/FC融合蛋白和阿奇霉素可抑制在LPS刺激下THP-1细胞TREM-1蛋白的表达,但对其基因表达无抑制作用;二者还可明显抑制炎性细胞因子的分泌,与LPS组比较,差异均有统计学意义(P<0.01),且TREM-1/FC融合蛋白的抑制作用强于阿奇霉素。结论 TREM-1是调控炎症反应及感染性疾病的重要靶点;阿奇霉素对TREM-1具有调节作用,为其进一步的临床研究提供了实验依据。
Objective To investigate the regulatory effect of azithromycin on human leukemia cell line THP-1 myeloid cells-1 (TREM-1) stimulated by lipopolysaccharide (LPS) and the effect of TREM- 1 regulation of the significance of the inflammatory response. Methods THP-1 cells were divided into LPS group (1μg / ml LPS), LPS + TREM-1 / FC fusion protein group (1μg / ml LPS and 1μg / ml TREM-1 / FC fusion protein) and LPS + azithromycin (1 μg / ml LPS and 10 μg / ml azithromycin was added). After cultured for 4, 8, 12, 24 and 48 h, the expression of TREM-1 mRNA and protein in each group were detected by RT-PCR and Western blot respectively. The soluble TREM (Soluble TREM-1, sTREM-1), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin- (Interleukin-1β, IL-1β) levels. Results TREM-1 / FC fusion protein and azithromycin could inhibit the expression of TREM-1 protein in LPS-stimulated THP-1 cells but did not inhibit the expression of TREM-1 protein. Both of them also significantly inhibited the secretion of inflammatory cytokines, LPS group, the differences were statistically significant (P <0.01), and TREM-1 / FC fusion protein inhibition stronger than azithromycin. Conclusion TREM-1 is an important target for the regulation of inflammatory and infectious diseases. Azithromycin has a regulatory effect on TREM-1 and provides an experimental basis for its further clinical research.