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

To explore the effect of atractylenolide-1 (ATL-Ⅰ) on alveolar macrophages in silicosis patients. 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. 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 (<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 (<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 (>0.05) . There was no statistically significant differences in the expression of the above indexes between the control group and DMSO group (>0.05) . 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.