文章摘要
赵 明,宋 勇,戴 伟,吕镗烽,刘红兵,辛晓峰,张剑雅.NLRP3炎症小体表达与慢性阻塞性肺疾病合并肺癌的相关性研究[J].,2019,19(8):1436-1440
NLRP3炎症小体表达与慢性阻塞性肺疾病合并肺癌的相关性研究
A Study on the Correlation between the Expression of NLRP3 Inflammasome and Chronic Obstructive Pulmonary Disease Combined with Lung Cancer
投稿时间:2018-09-05  修订日期:2018-10-09
DOI:10.13241/j.cnki.pmb.2019.08.008
中文关键词: 慢性阻塞性肺疾病  肺癌  NLRP3  炎症小体  相关性
英文关键词: Chronic obstructive pulmonary disease  Lung cancer  NLRP3  Inflammasome  Correlation
基金项目:江苏省自然科学基金(面上)项目(BK20161386);国家自然科学基金(面上) 项目(81772500)
作者单位E-mail
赵 明 海军军医大学南京临床学院 南京总医院 呼吸内科 江苏 南京 210002 zhaaoming@163.com 
宋 勇 海军军医大学南京临床学院 南京总医院 呼吸内科 江苏 南京 210002  
戴 伟 海军军医大学南京临床学院 南京总医院 呼吸内科 江苏 南京 210002  
吕镗烽 海军军医大学南京临床学院 南京总医院 呼吸内科 江苏 南京 210002  
刘红兵 海军军医大学南京临床学院 南京总医院 呼吸内科 江苏 南京 210002  
辛晓峰 海军军医大学南京临床学院 南京总医院 呼吸内科 江苏 南京 210002  
张剑雅 海军军医大学南京临床学院 南京总医院 呼吸内科 江苏 南京 210002  
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中文摘要:
      摘要 目的:分析核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体表达与慢性阻塞性肺疾病(COPD)合并肺癌的相关性。方法:选取2015年1月-2018年2月我院收治的COPD合并肺癌患者62例作为实验组及同期88例COPD患者作为对照组。酶联免疫吸附法(ELISA)检测两组患者外周血IL-1β、IL-18浓度,免疫组化法检测两组患者术后肺病理组织中Caspase-1、ASC、NLRP3、IL-1β、IL-18蛋白相对表达量,并比较不同病理特征下患者术后肺病理组织中NLRP3、ASC、Caspase-1、IL-1β、IL-18蛋白相对表达量的差异,并分析其与COPD合并肺癌的相关性。结果:实验组患者外周血IL-1β、IL-18水平均明显高于对照组,差异具有统计学意义(P<0.05);实验组患者术后肺病理组织中NLRP3、ASC、Caspase-1、IL-1β、IL-18蛋白相对表达量均明显高于对照组,差异均具有统计学意义(P<0.05);中低分化、临床分期Ⅲ期、淋巴结有转移的急性加重期COPD合并肺癌患者术后肺病理组织中NLRP3、ASC、Caspase-1、IL-1β、IL-18蛋白相对表达量高于高分化、临床分期Ⅰ-Ⅱ期、淋巴结无转移的稳定期COPD合并肺癌患者,差异具有统计学意义(P<0.05)。经Spearman秩相关性分析发现,患者术后肺病理组织中NLRP3、ASC、Caspase-1、IL-1β、IL-18蛋白相对表达量与COPD合并肺癌患者病情严重程度、淋巴结转移情况、分化程度以及病情所处时期均呈正相关(r>0,P<0.05)。结论:NLRP3炎症小体通路可能参与了COPD合并肺癌的发展过程,其释放的细胞因子IL-1β、IL-18水平升高可能与患者持续炎症有关,并进一步导致机体免疫病理损伤,促进疾病进展。
英文摘要:
      ABSTRACT Objective: To analyze the correlation between the nucleotide binding oligomerization domain like receptor protein 3 (NLRP3) inflammasome expression and chronic obstructive pulmonary disease (COPD) combined with lung cancer. Methods: 62 patients with COPD and lung cancer admitted in the hospital from January 2015 to February 2018 were selected as experimental group, and 88 COPD patients were selected as control group at the same time. The concentration of peripheral blood interleukin-1β (IL-1β) and interleukin-18 (IL-18) in the two groups were detected by enzyme-linked immunosorbent assay (ELISA). The relative expression of Caspase-1, ASC, NLRP3, IL-1β, IL-18 protein in the postoperative pulmonary pathological tissues of the two groups were detected by immunohistochemistry. The difference in the relative expression of NLRP3, ASC, Caspase-1, IL-1β and IL-18 protein in the postoperative pulmonary pathological tissues of patients with different pathological features was compared, and its correlation with COPD and lung cancer was analyzed. Results: The results of ELISA showed that: the levels of peripheral blood IL-1β and IL-18 in experimental group were significantly higher than those in control group (P<0.05); The relative expression of NLRP3, ASC, Caspase-1, IL-1β and IL-18 protein in the postoperative pulmonary pathological tissues in experimental group were significantly higher than those in control group (P<0.05); The relative expression of NLRP3, ASC, Caspase-1, IL-1β, IL-18 protein in the postoperative pulmonary pathological tissues in the acute exacerbation of COPD and lung cancer patients with histological type of moderate and low differentiation, clinical stage III, lymph node metastasis were higher than those in the stable COPD and lung cancer patients with histological type of high-differentiation, clinical stage I-II, without lymph node metastasis (P<0.05); Spearman rank correlation analysis showed that the relative expression of NLRP3, ASC, Caspase-1, IL-1β, IL-18 protein in the postoperative pulmonary pathological tissues of patients had positive correlation with the severity of disease, lymph node metastasis, degree of differentiation, staging of disease in COPD and lung cancer patients (r>0. P<0.05). Conclusion: NLRP3 inflammasome pathway may be involved in the development of COPD combined with lung cancer. The elevated levels of released cytokines such as IL-1β and IL-18 may be associated with the persistent inflammation of patients, and further lead to immune pathological damage and promote disease progression.
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