Objective: To investigate the effect of smoking on autophagy in alveolar macrophages (AMs) of silicosis patients. Methods: In December 2019, a random sampling method was used to select 42 male patients with silicosis (19 cases of stage II and 23 cases of stage III) who were treated with large volume whole lung lavage from August to December 2017 in the Beidaihe sanatorium. According to the different smoking index of the study subjects (smoking index=smoking cigarette consumptions per day×years of smoking) , we divided them into high (Smoking index>400) , medium (200≤smoking index≤400) , low (smoking index <200) and non-smoking group. The levels of autophagy related proteins LC3, Beclin1, p62 and apoptosis related protein Cleaved Caspase-3 were detected by Western blot. The effects of smoking on autophagy activity of AMs in silicosis were analyzed. Results: The ratio of autophagy related protein LC3 II/LC3 I, the expression of Beclin1, p62, and apoptosis related protein Cleaved Caspase-3 in the high smoking group were significantly higher than that of the middle, low smoking group and the non-smoking group (P<0.05) . Conclusion: Smoking can aggravate the dysfunction of autophagic degradation in silicosis patients' AMs, which may accelerate the progress of silicosis through increasing apoptosis in AMs.
目的： 探讨吸烟对矽肺患者肺泡巨噬细胞（AMs）自噬的影响。 方法： 2019年12月，采用随机抽样选择2017年8至12月在中国煤矿工人北戴河疗养院进行治疗并行大容量全肺灌洗术的42例男性矽肺患者（矽肺贰期19例、叄期23例）作为调查对象。根据其吸烟指数的不同（吸烟指数=每天吸烟支数×吸烟年数），将其分为高（吸烟指数>400）、中（200≤吸烟指数≤400）、低（吸烟指数<200）以及不吸烟组，采用蛋白免疫印迹（Western blotting）方法检测各组自噬相关蛋白微管相关蛋白轻链3（LC3）、Beclin1、p62和凋亡相关蛋白Cleaved Caspase-3的表达水平，分析吸烟对矽肺患者肺泡巨噬细胞自噬活动的影响。 结果： 与中、低吸烟组和不吸烟组比较，高吸烟组自噬相关蛋白LC3Ⅱ/LC3Ⅰ比值、Beclin1、自噬降解底物蛋白p62、凋亡相关蛋白Cleaved Caspase-3的表达均升高，差异均有统计学意义（P<0.05）。 结论： 吸烟可加重矽肺患者AMs自噬降解障碍，可能通过加重AMs凋亡加速矽肺纤维化的发病进程。.
Keywords: Alveolar macrophages; Autophagy; Silicosis; Smoking.