ARHGAP24 ameliorates inflammatory response through inactivating Rac1/Akt/NF-κB pathway in acute pneumonia model of rat.
ARHGAP24 ameliorates inflammatory response through inactivating Rac1/Akt/NF-κB pathway in acute pneumonia model of rat.
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DOI：
10.21037/atm-20-5000
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发表时间：
2020-10
影响因子：
--
通讯作者：
Zuo Y
中科院分区：
文献类型：
--
作者：
Liu H;Wang W;Shen W;Wang L;Zuo Y
ARHGAP 24可能在急性肺炎的发生发展中发挥保护作用，但其机制仍是一个谜。本研究以大鼠急性肺炎模型为研究对象，探讨ARHGAP 24的作用机制。采用Western blotting法检测大鼠绿脓杆菌急性肺炎模型12、24、36、48 h后ARHGAP 24的表达。在大鼠急性肺炎模型中，分别检测肺组织病理学改变、肺水肿和支气管肺泡灌洗液（BALF）中炎性细胞因子水平，综合评价腺病毒介导ARHGAP 24过表达的有益作用。Western blotting分析ARHGAP 24过表达对Rac 1/Akt/NF-κB通路相关蛋白表达的影响。我们发现，在大鼠急性肺炎模型中，绿脓杆菌处理12、24、36和48 h后，ARHGAP 24的表达趋于降低。免疫印迹和免疫组织化学染色结果显示，转染ARHGAP 24的大鼠中ARHGAP 24高表达，并出现大量的ARHGAP 24阳性区域。同时，ARHGAP 24的过表达通过减轻肺组织病理学恶化、肺水肿和肺BALF中炎性细胞因子的水平来抑制急性肺炎的发展。更重要的是，ARHGAP 24过表达抑制了Rac 1、Akt和NF-κB的激活。因此，我们认为ARHGAP 24通过抑制Rac 1/Akt/NF-κB通路，减轻了大鼠急性肺炎模型的炎症反应。
ARHGAP24 might play a protective effect in the development of acute pneumonia, but the underlying mechanism remained a mystery. We aimed to investigate the effect of ARHGAP24 and explore the protective mechanism based on the acute pneumonia model of rats. Western blotting analysis was conducted to measure the expression of ARHGAP24 in the rat model of bacillus pyocyaneus-induced acute pneumonia after 12, 24, 36, and 48 h modeling. In the acute pneumonia model of rat, lung histopathological change, lung edema, and levels of inflammatory cytokines in the broncho alveolar lavage fluid (BALF) were respectively measured to comprehensively evaluate the beneficial effect of overexpression of ARHGAP24 mediated by adenovirus. The western blotting analysis was conducted to evaluate Rac1/Akt/NF-κB pathway-related protein expression change with ARHGAP24 overexpression. We found that ARHGAP24 expression tended to be lower in the acute pneumonia model of the rat after bacillus pyocyaneus treated 12, 24, 36, and 48 h. High expression of ARHGAP24 and a substantial ARHGAP24 positive area was found in the western blotting analysis and immunohistochemical staining in rats transfected with ARHGAP24. In the meantime, overexpression of ARHGAP24 suppressed the development of acute pneumonia through alleviating lung histopathological deterioration, lung edema, and levels of inflammatory cytokines in the BALF of the lung. What is more critical, ARHGAP24 overexpression inhibits the activation of Rac1, Akt, and NF-κB. Thus, we conclude that ARHGAP24 ameliorated the inflammatory response in the acute pneumonia model of the rat through inactivating the Rac1/Akt/NF-κB pathway.
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影响因子：
3.7
作者：
Dietert K;Gutbier B;Wienhold SM;Reppe K;Jiang X;Yao L;Chaput C;Naujoks J;Brack M;Kupke A;Peteranderl C;Becker S;von Lachner C;Baal N;Slevogt H;Hocke AC;Witzenrath M;Opitz B;Herold S;Hackstein H;Sander LE;Suttorp N;Gruber AD
通讯作者：
Gruber AD
DOI：
10.4049/jimmunol.1602090
发表时间：
2018-04-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Sham HP;Walker KH;Abdulnour RE;Krishnamoorthy N;Douda DN;Norris PC;Barkas I;Benito-Figueroa S;Colby JK;Serhan CN;Levy BD
通讯作者：
Levy BD
Dapk1 通过 p38MAPK/NF-κB 信号通路改善 LPS 诱导的急性肺损伤中的炎症、氧化应激和自噬
影响因子：
3.6
作者：
Li, Tao;Wu, Yi-Na;Duan, Jun
通讯作者：
Duan, Jun
DOI：
10.1152/ajplung.00200.2013
发表时间：
2014-04-01
影响因子：
4.9
作者：
Pirot, Nelly;Delpech, Helene;Pinet, Valerie
通讯作者：
Pinet, Valerie
影响因子：
5.3
作者：
Schauer, Anja E.;Klassert, Tilman E.;Slevogt, Hortense
通讯作者：
Slevogt, Hortense