| 郭晓雅,宋立强,梁家宁,杨学敏,陈 洁.干预气道杯状细胞CLCA对ARDS小鼠损伤程度及炎症机制的影响[J].现代生物医学进展英文版,2019,19(5):824-828. |
| 干预气道杯状细胞CLCA对ARDS小鼠损伤程度及炎症机制的影响 |
| Effects of Intervention Airway Goblet Cell CLCA on the Injury Degree and Inflammatory Mechanism of ARDS mice |
| Received:September 04, 2018 Revised:September 28, 2018 |
| DOI：10.13241/j.cnki.pmb.2019.05.006 |
| 中文关键词: ARDS 气道上皮杯状细胞 钙激活氯离子通道蛋白 |
| 英文关键词: ARDS Airway goblet cells CLCA |
| 基金项目:国家自然科学基金面上项目（81570072） |
| Author Name | Affiliation | E-mail | | GUO Xiao-ya | Department of Respiratory Medicine, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | guoxiaoya0827@126.com | | SONG Li-qiang | Department of Respiratory Medicine, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | | | LIANG Jia-ning | Department of Respiratory Medicine, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | | | YANG Xue-min | Department of Respiratory Medicine, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | | | CHEN Jie | Department of Respiratory Medicine, Xijing Hospital, Air Force Military Medical University, Xi'an, Shaanxi, 710032, China | |
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| 中文摘要: |
| 摘要 目的：探讨干预气道杯状细胞CLCA的表达与功能，对ARDS小鼠肺脏损伤程度的影响，并通过体外细胞研究探讨其机制。方法：制备LPS诱导的ARDS小鼠模型（ARDS组），并在此模型上分别进行干预，包括气道雾化吸入CLCA非特异性阻断剂尼氟灭酸（NFA）（NFA+ARDS组）、气道滴注CLCA特异性抗体（ab-CLCA3）（ab-CLCA3+ARDS组）。HE染色观察各组小鼠肺部病理及炎症特征，计算肺损伤评分。运用hCLCA1-siRNA抑制人正常支气管上皮细胞系16HBE中hCLCA1的表达，采用real-time RT-PCR法验证抑制效果后，检测各组细胞合成多种炎症因子mRNA水平的差异。结果：HE染色显示，ARDS组与NFA+ARDS组相比，肺部病理改变及炎症细胞浸润程度无明显差异，肺损伤评分也没有统计学差异（正常组：2.0±0.71；ARDS组：6.8±0.45，NFA+ARDS组7.4±0.89，P>0.05）。与ARDS组相比，ab-CLCA3+ARDS组肺部病理损伤及炎症细胞浸润程度明显加重，肺损伤评分也升高（正常组：1.8±0.83；ARDS组：7.6±0.55，ab-mCLCA3+ARDS组9.8±0.83，P<0.05）。real-time RT-PCR检测证实成功构建hCLCA1低表达的16HBE细胞系，同时real-time RT-PCR结果显示TNF-α和IL-1β的mRNA表达水平升高（P<0.05）。结论：阻断气道CLCA功能区域，可以加重ARDS小鼠肺部病理损伤程度及炎症细胞浸润水平，提示气道杯状细胞CLCA在ARDS小鼠肺部炎症形成过程中发挥抑制性调节作用。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect of interfering with the expression and function of CLCA in airway goblet cells to the lung injury degree of ARDS mice, and to explore its mechanism through cell research. Methods: The lipopolysaccharide(LPS) in- duced ARDS mice through trachea drip.HE staining was employed to observe pulmonary inflammatory cell infiltration and pathological change of the lung tissue in mice challenged NFA or mCLCA3 antibody. Real-time RT-PCR was used to test the mRNA and the protein expression levels of hCLCA1 in 16-HBE cell lines, which were transfected hCLCA1-Si-RNA. Real-time RT-PCR was used to examine the mRNA expression levels of multiple inflammatory factors. Results: HE staining showed that there was no different between NFA mice and control mice in the levels of lung tissue inflammation infiltration(Control group: 2.0±0.71; ARDS group: 6.8±0.45; NFA+ARDS group: 7.4±0.89, P>0.05). However, the infiltration degree of lung tissue inflammation infiltration is more noticeable in mice administrated mCLCA3 antibody than the ARDS group(Control group: 1.8±0.83; ARDS group: 7.6±0.55; ab-mCLCA3+ARDS group: 9.8±0.83,P<0.05). Real-time RT-PCR results confirmed that there was a significant reduce in the mRNA expression levels of hCLCA1 in 16-HBE cell lines transfected hCLCA1-Si-RNA, revealling a successful suppressed of hCLCA1 in 16-HBE cell lines. And Real-time RT-PCR re- sults showed that the mRNA expression levels of TNF-α and IL-1β increased obviously in 16-HBE cell lines（P<0.05). Conclusion: The decrease of mCLCA3 can aggravate the lung pathological damage degree and the pulmonary inflammatory response in ARDS mice. These results revealed that CLCA secreted by airway goblet cells inhibit the inflammatory response in the process of ARDS. |
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