ARHGAP24 ameliorates inflammatory response through inactivating Rac1/Akt/NF-κB pathway in acute pneumonia model of rat.

BACKGROUND

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.