Inflammation can cause a series of inflammatory
lung disease, which seriously endangers human health.
Pulmonary fibrosis is a kind of inflammatory disease with end-stage lung pathological changes. It has complicated and unknown pathogenesis and is still lack of effective therapeutic drugs. LPS-induced
inflammation is a common feature of many infectious
inflammations such as
pneumonia,
bacteremia,
glomerulonephritis, etc.
Evodiamine, one of the main components of Evodia rutaecarpa, is an
alkaloid with excellent antiinflammatory effects. In this study, we evaluated the protective capacities of
evodiamine on LPS-induced inflammatory damages in vitro and in vivo. MTT method, flow cytometry, immunofluorescence, and other methods were used for in vitro study to determine the protective capacities of
evodiamine. The results suggest that
evodiamine can protect murine macrophages from the LPS-
nigericin-induced damages by (a) inhibiting cellular apoptosis, (b) inhibiting inflammatory
cytokines releasing, and (c) activating the
apelin pathway. We also used the exogenous
apelin-13 peptide co-cultured with LPS-
nigericin in RAW264.7 cells and found that
apelin-13 contributes to protecting the effects of
evodiamine. In vivo, the ELISA method and immunohistochemistry were used to examine inflammatory
cytokines,
apelin, and histological changes. BALB/c mice were exposed to LPS and subsequent administration of
evodiamine (p.o.)for some time, the results of the alveolar lavage fluid and the tissue slices showed that
evodiamine treatment alleviated the
pulmonary inflammation and
fibrosis, stimulated
apelin expression and inhibited the inflammatory
cytokines. These results provide a basis for the protective effect and mechanism of
evodiamine in LPS-induced
inflammation and suggest that it might be potential
therapeutics in human pulmonary
infections.