Background:Acute lung injury (ALI) is a serious lung disease characterized by acute
and severe inflammation. Upregulation of ACE2 and inhibition of the NF-κB signaling pathway
attenuate LPS-induced ALI.Objective:To explore whether Zang Siwei Qingfei Mixture inhibits the development of ALI
through the ACE2/NF-κB signaling pathway.Methods:Alveolar type II epithelial cells (AEC II) were identified by immunofluorescence staining
and flow cytometry. C57BL/6J mice were treated with LPS to establish an ALI model. Cell viability
was assessed using CCK8 assays. The levels of ACE, ACE2, p-p38/p38, p-
ERK1/2/ERK1/2, p-JNK/JNK, p-IκBα/IκB-α, p-NF-κBp65 were analyzed by Western blotting.
ELISA was applied to detect the levels of TNF-a, IL-6, AGT, and Ang1-7. HE staining was used to
observe lung injury. The mRNA expression of ACE, ACE2, and Mas was measured by RT-qPCR.Results:AEC II cells were successfully isolated. Treatment with the Zang Siwei Qingfei Mixture
resulted in a decrease in ACE, p-p38/p38, p-ERK1/2/ERK1/2, p-JNK/JNK, p-IκBα/IκB-α,
p-NF-κBp65 levels, while increasing ACE2 levels. Zang Siwei Qingfei mixture also led to a reduction
in TNF-α, IL6, and AGT levels, while increasing Ang1-7 level. Histological analysis
showed that Zang Siwei Qingfei Mixture treatment improved the alveolar structure of ALI mice
and reduced inflammatory infiltration. The pretreatment with MLN-4760, an ACE2 inhibitor,
resulted in opposite effects compared to Zang Siwei Qingfei Mixture treatment.Conclusion:Zang Siwei Qingfei mixture attenuates ALI by regulating the ACE2/NF-κB signaling
pathway in mice. This study provides a theoretical foundation for the development of improved
ALI treatments.