Kangaoheji Relieves Acute Lung Injury through p38 MAPK/NF-κB Signaling Pathway and ACE2/Ang1-7/Mas Axis
OBJECTIVE To explore the effect and mechanism of Kangaoheji(KAHJ)in the treatment of acute lung injury(ALI)in mice,and provide a rationale for its possible use as a drug to alleviate symptoms following coronavirus disease 2019(COV-ID-19)infection.METHODS Network pharmacology was carried out to predict the main active components and potential targets of KAHJ on ALI.C57BL/6J mice were randomly divided into Control group,LPS group and LPS+KAHJ group.LPS+KAHJ group was gavaged with KAHJ(4.76 g·kg-1·d-1,8.8 mL·kg-1·d-1)and the rest of the groups were gavaged with saline(8.8 mL·kg-1·d-1).LPS(5 mg·kg-1)was injected intraperitoneally to induce an acute inflammation model after 14 d.The ser-um and lung tissues of mice were collected,and the pathological changes in lung tissues were observed via histopathology.Western blot,Real-time PCR,Enzyme-Linked immunosorbent assay(ELISA)and immunohistochemistry(IHC)were used to assess the a-meliorative effect of KAHJ on ALI.RESULTS The result showed that 70 core target genes of KAHJ on ALI were primarily implicated in multiple signaling pathways involving MAPK signaling pathway,NF-κB signaling pathway,apoptosis,and Ras signaling pathway.Furthermore,we found that KAHJ ameliorated inflammation and apoptosis in ALI,thereby reducing lung damage and pulmo-nary edema and inhibiting pulmonary fibrosis.Additionally,KAHJ inhibited the phosphorylation of p38 MAPK and NF-κB,and up-regulated the ACE2/Ang1-7/Mas axis.CONCLUSION KAHJ might relieve acute lung injury through p38 MAPK/NF-κB signaling pathway and ACE2/Ang1-7/Mas axis,which offers complementary and alternative treatment options for COVID-19.
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维普
