Efficacy of mesenchymal stem cells mitigating VAP-induced lung injury by inhibiting PI3K/Akt signaling pathway
Objective Ventilator-associated pneumonia(VAP)is the most common infectious disease in mechanically ventilated patients,which seriously decreases the prognosis of critically ill patients,but its pathogenesis is still unclear.This study investigated the effect of mesenchymal stem cells(MSCs)on the inflammatory response of alveolar epithelial cells during VAP development.Methods This study was conducted from May 2020 to March 2023.In this study,VAP rat animal model was established and MSCs were extracted and identified.Fifteen rats were randomly divided into 3 groups:a control group,a VAP group,and a VAP+MSCs group.The alveolar epithelial cells of the control group and the VAP group were cultured alone in the incubator,and the alveolar epithelial cells of the VAP+MSCs group were co-cultured with the MSCs in the incubator.After 48 hours,the expressions of phosphatidylinositol 3-kinase(PI3K),serine/threonine protein kinase(Akt),and downstream inflammatory factors[tumor necrosis factor-α(TNF-α),interleukin-1α(IL-1α),and γ-interferon(IFN-y)]were detected by real-time fluorescence quantitative nucleic acid amplification assay(qPCR)and enzyme-linked immunosorbent assay(ELISA).Independent sample t test and one-way analysis of variance were used.Results The results of qPCR and ELISA showed that the expression levels of PI3K,Akt,and downstream inflammatory factors(TNF-α,IL-1α,and IFN-y)were the lowest in the control group;the mRNA expression levels of PI3K,Akt,and downstream inflammatory factors(TNF-α,IL-1α,and IFN-γ)in the VAP group were higher than those in the other two groups;the levels of inflammatory factors in the VAP+MSCs group were higher than those in the control group,but were lower than those in the VAP group,with statistically significant differences(all P＜0.05).Conclusion MSCs may inhibit the inflammatory factor expression in alveolar epithelial cells by inhibiting the PI3K/Akt signaling pathway,thus achieving the inhibition or mitigation of VAP.
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