文章摘要
祁晶晶,刘燕坤,薛 冰,湛文博,景博琼,姜 华.NLRP3炎症小体对克雷伯杆菌肺炎小鼠肺脏病理损伤的调节作用[J].,2022,(10):1825-1828
NLRP3炎症小体对克雷伯杆菌肺炎小鼠肺脏病理损伤的调节作用
Regulation of NLRP3 Inflammasome on Lung Pathological Damage in Mice with Klebsiella Pneumonia
投稿时间:2021-10-11  修订日期:2021-10-31
DOI:10.13241/j.cnki.pmb.2022.10.006
中文关键词: 克雷伯杆菌  肺炎  含NLR家族PYRIN域蛋白3  炎症小体  肺脏病理损伤  髓过氧化酶
英文关键词: Klebsiella  Pneumonia  NLR family PYRIN domain protein 3  Inflammasome  Lung pathological damage  Myeloperoxidase
基金项目:新疆维吾尔自治区自然科学基金项目(2019D01C131)
作者单位E-mail
祁晶晶 新疆医科大学第五附属医院检验科 新疆 乌鲁木齐 830011 jingjing21109@163.com 
刘燕坤 伊宁海关技术中心卫生检疫实验室 新疆 伊宁 835000  
薛 冰 新疆医科大学第五附属医院检验科 新疆 乌鲁木齐 830011  
湛文博 新疆医科大学第五附属医院检验科 新疆 乌鲁木齐 830011  
景博琼 新疆医科大学第五附属医院检验科 新疆 乌鲁木齐 830011  
姜 华 新疆医科大学第五附属医院重症监护室 新疆 乌鲁木齐 830011  
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中文摘要:
      摘要 目的:探讨含NLR家族PYRIN域蛋白3(NLR family pyrin domain containing 3,NLRP3)炎症小体对克雷伯杆菌肺炎小鼠肺脏病理损伤的调节作用。方法:56只C57BL/6小鼠随机平分为两组-模型组与对照组,模型组小鼠通过气管注射肺炎克雷伯杆菌建立克雷伯杆菌肺炎模型,对照组小鼠注射等体积的生理盐水,记录与观察肺脏病理损伤情况。结果:模型组建模第7 d与第14 d的肺泡灌洗液髓过氧化酶(Myeloperoxidase,MPO)活性都高于对照组(P<0.05)。模型组建模第7 d与第14 d的肺脏、脾脏、肝脏系数与肺脏病理评分、NLRP3蛋白相对表达水平都高于对照组(P<0.05)。在模型组中,建模第14 d的NLRP3蛋白相对表达水平与肺脏病理评分、肺脏系数、脾脏系数、肝脏系数、肺泡灌洗液MPO活性都存在正相关性(P<0.05)。结论:克雷伯杆菌肺炎小鼠NLRP3炎症小体呈现高表达状况,可介导小鼠肺脏病理损伤,促进MPO活性增加,加重多脏器损伤。
英文摘要:
      ABSTRACT Objective: To investigate the regulatory effect of inflammasomes containing NLR family pyrin domain containing 3 (NLRP3) on lung pathological damage in mice with Klebsiella pneumonia. Methods: 56 cases of C57BL/6 mice were randomly divided into two groups-model group and control group. The model group mice were injected with Klebsiella pneumoniae through the trachea to establish Klebsiella pneumonia models, and the control group mice were injected with an equal volume of physiology salt water, recorded and observed lung pathological damage. Results: The myeloperoxidase (MPO) activity of the alveolar lavage fluid on the 7th and 14th days of the model group were higher than that of the control group (P<0.05). The lung, spleen, liver coefficient, lung pathological score, and relative expression levels of NLRP3 protein on the 7th and 14th days of modeling in the model group were higher than those in the control group (P<0.05). In the model group, the relative expression level of NLRP3 protein on the 14th day of modeling were positively correlated with lung pathology score, lung coefficient, spleen coefficient, liver coefficient, and MPO activity of alveolar lavage fluid (P<0.05). Conclusion: The NLRP3 inflammasome of mice with Klebsiella pneumonia are highly expressed, which can mediate pathological damage of lungs in mice, promote the increase of MPO activity, and aggravate multiple organ damage.
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