Effects of leonzurine on LPS-induced inflammatory injury of alveolar epithelial cells by regulating the MCP-1/CCR2 axis
Objective To investigate the effect of leonzurine(Leo)on lipopolysaccharide(LPS)-induced inflammatory injury of alveolar epithelial cells by regulating the monocyte chemoattractant protein 1(MCP-1)/CC chemokine receptor 2(CCR2)axis.Methods The human alveolar epithelial cells(AECs)were cultured in vitro.They were induced with blank control,10μg/mL LPS,LPS + low-dose Leo at 10μmol/L,LPS + medium-dose Leo at 20μmol/L,LPS + high-dose Leo at 30μmol/L,LPS + MCP-1 activator SLIGKV at 50μmol/L,and LPS + high-dose Leo + SLIGKV.Cell proliferation and apoptosis were detected by CCK-8 assay and flow cytometry,respectively.Relative levels of interleukin 2(IL-2)and tumor necrosis factor-α(TNF-α)in the cell supernatant were measured by enzyme linked immunosorbent assay(ELISA).Real-time fluorescence quantitative PCR(qRT-PCR)and Western blot were applied to detect the expression levels of key genes in the MCP-1/CCR2 signaling pathway and apoptotic proteins.Results Compared with those of blank control,LPS-induced AECs presented significantly higher apoptotic rate and expression levels of MCP-1,CCR2,IL-2,TNF-α and Bcl-2-associated X protein(Bax),and significantly lower optical density at 450 nm(OD450)and expression level of B-cell lymphoma-2(Bcl-2)(P<0.05).Compared with those induced with LPS,LPS-induced AECs treated with low-dose,medium-dose and high-dose Leo presented significantly lower apoptotic rate and expression levels of MCP-1,CCR2,IL-2,TNF-α and Bax,and significantly higher OD450 and expression level of Bcl-2 in a dose-dependent manner(P<0.05).Opposite trends were detected in LPS-induced cells treated with SLIGKV,which weakened the protective effect of high-dose Leo on LPS-induced inflammatory injury of AECs.Conclusion Leo alleviates LPS-induced inflammatory damage to alveolar epithelial cells by inhibiting the MCP-1/CCR2 axis.
leonurinelipopolysaccharidemonocyte chemoattractant protein 1/CC chemokine receptor 2 signal axispulmonary alveolar epithelial cellsproliferationapoptosisinflammation
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