目的 探讨自噬、中性粒细胞凋亡和中性粒细胞外泌网（NET）形成在全身性红斑狼疮（SLE）中的作用。 方法 共招募36例SLE患者作为研究对象，招募相应匹配的32名健康对照作为对照对象。通过Western blot分析检测中性粒细胞中微管相关蛋白1轻链3B（LC3B）、自噬相关基因5（ATG5）、P62、B细胞淋巴瘤2（Bcl2）、Bcl2相关X蛋白（BAX）的表达水平。采用流式细胞术分析中性粒细胞上LC3B的表达。通过ELISA估计血浆中过氧化物酶（MPO）的表达水平。此外，将中性粒细胞体外培养，并分别用100 nmol/L雷帕霉素和10 μg/mL脂多糖（LPS）刺激6小时。随后，通过Western blot分析检测中性粒细胞中LC3B、ATG5、P62、Bcl2和BAX的表达水平。采用ELISA检测培养上清中MPO的水平。采用SytoxTM Green染色结合荧光分光光度法测定培养上清中NET荧光强度的变化。 结果 与健康对照组相比，SLE患者的中性粒细胞自噬、凋亡和NET形成水平升高。凋亡和NET形成水平与中性粒细胞自噬呈正相关。受雷帕霉素刺激的中性粒细胞自噬水平升高，但对凋亡和NET形成没有影响。LPS诱导的中性粒细胞自噬和NET形成水平也增加，对凋亡没有显著影响。 结论 SLE患者的中性粒细胞自噬、凋亡和NET形成水平升高。中性粒细胞自噬和NET的激活可能是由SLE患者的炎症内部环境引起的。

Objective To explore the role of autophagy, apoptosis of neutrophils and neutrophils extracellular traps (NET) formation in systemic lupus erythematosus (SLE). Methods Thirty-six patients with SLE were recruited as research subjects, and 32 healthy controls matched accordingly were enrolled as control subjects. The expression levels of microtubule associated protein 1 light chain 3B (LC3B), autophagy-related gene5(ATG5), P62, B-cell lymphoma 2(Bcl2), Bcl2-related X protein (BAX) in neutrophils were detected by Western blot analysis. Flow cytometry was employed to analyze the expression of LC3B on neutrophils. The expression level of myeloperoxidase(MPO) in plasma was estimated by ELISA. Furthermore, neutrophils were cultured in vitro and stimulated by 100 nmol/L rapamycin and 10 μg/mL lipopolysaccharide (LPS) for 6 hours, respectively. And then, the expression levels of LC3B, ATG5, P62, Bcl2 and BAX in neutrophils were detected by Western blot analysis. The level of MPO in culture supernatant was detected by ELISA. The change of fluorescence intensity of NET in culture supernatant was assayed by SytoxTM Green staining combined with fluorescence spectrophotometry. Results Compared with healthy controls, the levels of autophagy and apoptosis of neutrophils and NET formation in SLE patients were increased. The level of apoptosis and NET formation was positively associated with neutrophil autophagy. The level of autophagy showed an increase but had no effect on apoptosis and NET formation for neutrophil stimulated by rapamycin. The levels of autophagy and NET formation also increased with no significant effect on apoptosis for neutrophil induced by LPS. Conclusion The autophagy, apoptosis and NET formation of neutrophils increase in SLE patients. The activation of autophagy and NET in neutrophils possibly result from the inflammatory internal environment in SLE patients.