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目的初步研究尘肺患者肺泡巨噬细胞(AM)的凋亡情况以及肿瘤坏死因子-α及其受体(TNF-α/TNFR)信号通路对AM凋亡的调控作用,为尘肺病的早期防治提供依据。方法选取30例尘肺患者为研究对象,收集其肺泡灌洗回收液,分离纯化AM,将实验分为5组,即未处理组、超氧化物歧化酶(SOD)组、TNF-α/TNFR组、抗-TNF-α组、半胱氨酰天冬氨酸特异蛋白(Caspase)-8抑制剂组。培养24h后,收获AM,分别用光学显微镜、透射电子显微镜、荧光共聚焦显微镜检测AM凋亡的情况。采用SAS8.2软件进行方差分析和2分析。结果光学显微镜、荧光共聚焦显微镜、透射电镜下均可见凋亡细胞染色质浓缩、边缘化、染色质分割成块状、核膜不完整和凋亡小体等典型的凋亡形态。SOD组、抗-TNF-α组、Caspase-8抑制剂组的AM凋亡指数均低于未处理组。结论尘肺患者AM存在一定程度的凋亡,表现为形态学的改变,凋亡程度与接尘性质有关,与尘肺期别、接尘工龄、脱尘年限无关。SOD复合酶、抗-TNF-α抗体、Caspase-8抑制剂可在信号通路的不同环节阻断信号转导,抑制AM凋亡的发生。
Objective To study the apoptosis of alveolar macrophages (AM) and the regulatory effect of tumor necrosis factor-α and its receptor (TNF-α / TNFR) signaling pathway on the apoptosis of pneumocytes in patients with pneumoconiosis. in accordance with. Methods Thirty patients with pneumoconiosis were enrolled in this study. The pulmonary alveolar lavage fluid was collected and purified. AM was divided into five groups: untreated group, superoxide dismutase (SOD) group and TNF-α / TNFR group , Anti-TNF-α group, Caspase-8 inhibitor group. After culturing for 24 hours, the AMs were harvested and the apoptosis of AM was detected by optical microscope, transmission electron microscope and fluorescent confocal microscope respectively. ANOVA and 2 analyzes were performed using SAS8.2 software. Results Apoptotic morphology of apoptotic cells such as chromatin condensation, marginalization, chromatin segmentalization, incomplete nuclear membrane and apoptotic bodies were observed under light microscope, fluorescence confocal microscope and transmission electron microscope. The apoptotic indexes of AM, anti-TNF-α and Caspase-8 inhibitor groups were lower than those of untreated group. Conclusion There is a certain degree of apoptosis of AM in pneumoconiosis patients, showing morphological changes. The degree of apoptosis is related to the nature of dust collection, and has no relation with the stages of pneumoconiosis, the age of dust collection and the age of dust removal. SOD complex enzyme, anti-TNF-α antibody and Caspase-8 inhibitor can block signal transduction in different parts of the signal pathway and inhibit the occurrence of AM apoptosis.