The protective role of fosfomycin in lung injury due to oxidative stress and inflammation caused by sepsis

Yıldız, İlknur Esen; Topçu, Atilla; Bahçeci, İ̇lkay; Arpa, Medeni; Tümkaya, Levent; Mercantepe, Tolga; Batçık, Şule; Yıldız, Yasin

doi:10.1016/j.lfs.2021.119662

Cited by 10 publications

(1 citation statement)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Currently, the most commonly used therapeutic drugs against ALI are antibiotics and glucocorticoids (Li et al., 2023). Several antibiotics, such as azithromycin, clarithromycin, and fosfomycin, inhibit NF‐κB activation in murine models of lung injury, thus exerting anti‐inflammatory effects (Amado‐Rodríguez et al., 2013; Stellari et al., 2014; Yildiz et al., 2021). Glucocorticoids have been widely used for ALI and its more severe form, acute respiratory distress syndrome (ARDS) (Guo et al., 2023).…”

Section: Discussionmentioning

confidence: 99%

The protective effect of karanjin against sepsis‐induced acute lung injury in mice is involved in the suppression of the TLR4 pathway

Zhang,

Ma,

Liu

et al. 2024

Chem Biol Drug Des

View full text Add to dashboard Cite

Sepsis‐induced acute lung injury (ALI) is a severe complication of sepsis. Karanjin, a natural flavonoid compound, has been proved to have anti‐inflammatory function, but its role in sepsis‐stimulated ALI is uncertain. Herein, the effect of karanjin on sepsis‐stimulated ALI was investigated. We built a mouse model of lipopolysaccharide (LPS)‐stimulated ALI. The histopathological morphology of lung tissues was scrutinized by hematoxylin–eosin (H&E) staining. The lung injury score and lung wet/dry weight ratio were detected. The myeloperoxidase (MPO) activity and malondialdehyde (MDA) content were scrutinized by commercial kits. Murine alveolar lung epithelial (MLE‐12) cells were treated with LPS to mimic a cellular model of ALI. The cell viability was scrutinized by the CCK‐8 assay. The contents of proinflammatory cytokines were scrutinized by qRT‐PCR and ELISA. The TLR4 and MyD88 contents were scrutinized by qRT‐PCR and western blotting. Results showed that karanjin alleviated LPS‐stimulated ALI in mice by inhibiting lung tissue lesions, edema, and oxidative stress. Moreover, karanjin inhibited LPS‐stimulated inflammation and TLR4 pathway activation in mice. However, treatment with GSK1795091, an agonist of TLR4, attenuated the effects of karanjin on LPS‐induced ALI. Furthermore, karanjin repressed LPS‐stimulated inflammatory response and TLR4 pathway activation in MLE‐12 cells. Overexpression of TLR4 attenuated karanjin effects on LPS‐stimulated inflammatory responses in MLE‐12 cells. In conclusion, karanjin repressed sepsis‐stimulated ALI in mice by suppressing the TLR4 pathway.

show abstract