Kaempferitrin alleviates LPS-induced septic acute lung injury in mice through downregulating NF-κB pathway

Background: Acute lung injury (ALI) causes severe and uncontrolled pulmonary inflammation and has high morbidity in dying patients. Objective: This study aimed to evaluate the potential function of Kaempferitrin (Kae) and uncover its mechanisms in ALI. Material and Methods: We evaluated the role of Kae in ALI through the lipopolysaccharide lavage fluid (BALF) cells count, pulmonary inflammation, and the levels of interleukin (IL)-6, tumor necrosis factor-alpha (TNF-alpha), and IL-1 beta. The effect of Kae on NF-kappa B signaling pathway was discovered through the protein expression levels of transcription factors p65, p-p65, I kappa B alpha, and p-I kappa B alpha by Western blot analysis. Results: The results showed that Kae could improve lung injury by reducing apoptosis, histopathological changes, and lung W/D ratio; more importantly, Kae enhanced the survival of ALI mice. Moreover, Kae relieved inflammation, as it reduced total BALF cells count, and deceased the levels of TNF-alpha, IL-6, and IL-1 beta in serum. In addition, Western blot analysis data suggested that Kae could decrease the protein expression levels of transcription factors p65, p-p65, I kappa B-alpha, and p-I kappa B-alpha, which were promoted by LPS. Conclusion: The results of this study suggested that Kae could relieve LPS-induced ALI in mice and reduce inflammation and apoptosis through NF-kappa B pathway. (c) 2023 Codon Publications. Published by Codon Publications.