[1]陈梅芳,林勇,张家欣,等.牵张离子通道通过miRNA-146a/NF-κB通路介导呼吸机相关性肺损伤的实验研究[J].福建医药杂志,2023,45(03):102-106.
　CHEN Meifang,LIN Yong,ZHANG Jiaxin,et al.Experimental study of stretch-activated channel contributing to ventilator-induced lung injury via miRNA-146a/NF-κB passway[J].FUJIAN MEDICAL JOURNAL,2023,45(03):102-106.
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牵张离子通道通过miRNA-146a/NF-κB通路介导呼吸机相关性肺损伤的实验研究()
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《福建医药杂志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期数:
2023年03期
页码:
102-106
栏目:
基础研究
出版日期:
2023-06-15

文章信息/Info

Title:
Experimental study of stretch-activated channel contributing to ventilator-induced lung injury via miRNA-146a/NF-κB passway
文章编号:
1002-2600(2023)03-0102-05
作者:
陈梅芳1; 林勇2; 张家欣; 吕晓钗; 王阶波3
福建医科大学附属协和医院心血管外科(福州 350001)
Author(s):
CHEN Meifang;  LIN Yong;  ZHANG Jiaxin;  LV Xiaochai;  WANG Jiebo
Department of Cardiovascular Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, China
关键词:
牵张离子通道;  呼吸机诱导肺损伤;  炎症
Keywords:
stretch-activated channels;  ventilator-induced lung injury;  inflammation
分类号:
R614.2; R654.2
文献标志码:
A
摘要:
目的 探析呼吸机相关性肺损伤(VILI)的发生机制,为防治VILI提供新的理论依据。方法 以自主呼吸大鼠为对照组(S组),大潮气量机械通气大鼠为实验组(V组),以牵张离子通道(SAC)阻滞剂大鼠作为干预措施组(V+B组),每组各12只; 机械通气后比较大鼠肺组织结构和功能、miRNA-146a、NF-κB P65、炎症因子(TNF-α、IL-6)表达有无不同。结果 机械通气后大鼠肺组织结构破坏明显,氧合功能明显减低,肺组织miRNA-146a表达明显下调,NF-κB P65表达上调,肺部和全身炎症因子浓度增加。相比V组大鼠,V+B组大鼠上述病变程度明显减轻,肺组织miRNA-146a表达下调减缓,NF-κB P65表达上调程度减轻,肺部和全身炎症因子浓度增加幅度减少。结论 SAC可能通过miRNA-146a/NF-κB途径介导VILI发生,有望成为防治VILI的新靶点。
Abstract:
Objective To explore the mechanism of ventilator-induced lung injury(VILI)and to provide some evidences for the prophylaxis and the treatment of VILI. Methods The mice were divided into three groups: spontaneous inspiration(group S), high tidal volume ventilation(group V), and high tidal volume ventilation with stretch-activated channels(SAC)blocker(group V+B)with each group 12 mice. Lung morphology and function, miRNA-146a expression,NF-κB P65 expression and inflammatory factors(TNF-α,IL-6) concentration in the serum and lung were evaluated in the setting of mechanical ventilation. Results Serious lesion in the lung with an obviously impaired oxygenation were observed in the mice that received high tidal volume ventilation. The expression of miRNA-146a significantly reduced, and the NF-κB P65 increased on the contrary. Serum and pulmonary inflammatory level elevated after ventilation. Compared with group V, morphology abnormity and oxygenation dysfunction relieved in the mice in the group V+B. Higher miRNA-146a level, lower NF-κB P65 expression and lower local and systemic inflammatory levels were observed in the mice of group V+B. Conclusion SAC contributes to VILI through the miRNA-146a/NF-κB passway and is expected to be a novel target for the prophylaxis and the treatment of VILI.

参考文献/References:

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备注/Memo

备注/Memo:
基金项目:福建省自然科学基金资助项目(2019J05082)
1 福建省心脏医学中心; 2 通信作者; 3 麻醉科
更新日期/Last Update: 2023-06-15