[The study of the impact by atractylenolide-1 on inflammatory cytokine, autophagy and apoptosis in alveolar macrophages of silicosis patients].

Objective: To explore the effect of atractylenolide-1 (ATL-Ⅰ) on alveolar macrophages in silicosis patients. Methods: In December 2019, 12 male silicosis patients treated in Beidaihe Sanatorium for Chinese Coal Miners from July to September 2019 were selected by random sampling. Their alveolar macrophages were collected and divided into control group, ATL-Ⅰ group (100 μmol/L) and dimethyl sulfoxide (DMSO) group (100 μmol/L) . The exprossion levels of inflammatory factor interleukin-1β (IL-1β) , interleukin-6 (IL-6) , tumor necrosis factor α (TNF-α) were detected by enzyme-linked immunosorbent assay. The expression levels of autophagy associated protein microtubule associated protein light chain 3 (LC3) , autophagy substrate protein p62, lysosome associated membrane protein 2 (LAMP2) , apoptosis associated protein Cleaved caspase-3, nuclear factor kappa B (NF-κB) and its phosphorylated form (p-NF-κB) were detected by Western blot. Results: Compared with the control group and DMSO group, the expression levels of IL-1β, IL-6, TNF-α in alveolar macrophages decreased significantly in the ATL-Ⅰ group (P<0.05) , and the expression levels of p-NF-κB, the ratio of LC3-Ⅱ/LC3-Ⅰ also decreased significantly in the ATL-Ⅰ group (P<0.05) . However, the expression levels of NF-κB, LAMP2, p62 and Cleaved caspase-3 in the ATL-Ⅰ group were not statistically different from those in the control group and DMSO group (P>0.05) . There was no statistically significant differences in the expression of the above indexes between the control group and DMSO group (P>0.05) . Conclusion: ATL-Ⅰ may reduce the release of inflammatory factors from alveolar macrophages and inhibit the activity of autophagy in silicosis patients, but it may not reduce the level of apoptosis.目的： 探究白术内酯-1（ATL-Ⅰ）对矽肺患者肺泡巨噬细胞的作用。 方法： 于2019年12月，利用随机抽样的方法，选择2019年7至9月在中国煤矿工人北戴河疗养院进行治疗的12例男性矽肺患者，收集其肺泡巨噬细胞分为对照组、ATL-Ⅰ组（100 μmol/L）以及二甲基亚砜（DMSO）组（100 μmol/L）。采用酶联免疫吸附试验检测炎症因子白细胞介素1β（IL-1β）、白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）的表达水平，用蛋白免疫印迹法检测自噬相关蛋白微管相关蛋白轻链3（LC3）、自噬底物蛋白p62、溶酶体关联膜蛋白2（LAMP2）、凋亡相关蛋白Cleaved caspase-3和核因子κB（NF-κB）及其磷酸化型（p-NF-κB）的表达水平。 结果： 与对照组和DMSO组比较，ATL-Ⅰ组肺泡巨噬细胞IL-1β、IL-6和TNF-α的表达明显降低（P<0.05），且p-NF-κB、LC3-Ⅱ/LC3-Ⅰ比值也明显降低（P<0.05）；但ATL-Ⅰ组NF-κB、LAMP2、p62以及Cleaved caspase-3表达与对照组和DMSO组差异均无统计学意义（P>0.05）；对照组与DMSO组的上述指标表达差异均无统计学意义（P>0.05）。 结论： ATL-1可能减少矽肺患者肺泡巨噬细胞炎症因子的释放，抑制自噬的活性，但未能降低其凋亡水平。.