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The aim of this study was to investigate the effects of emodin, the majorcomponent of Rheum palmatum, on lipopolysaccharide (LPS)-induced toll-like receptor4 (TLR4) expression in cultured mouse tubular epithelial cells (TECs). The TECswere obtained from mice and incubated with LPS and/or indicated concentrationsof emodin for 24 h. Cytokeratin, α-SMA and vimentin were detected using immunohistochemistry.The TLR4 protein level was detected by flow cytometry. TNFα and IL-6 protein levelswere measured using an enzyme-linked immunosorbent assay (ELISA). mRNA expressionof TLR4, TNFα and IL-6 was detected using a reverse-transcription polymerase chainreaction (RT-PCR). Results showed that a concentration of 102 ng/ml LPS significantlyupregulated TLR4 mRNA and protein levels. TNFα and IL-6 mRNA and protein levelswere also increased. Emodin (at doses of 40, 20 and 10 µM) was able to inhibitLPS-induced TLR4 protein synthesis in cultured TECs. However, TNFα and IL-6 proteinexpression was decreased in cells treated with emodin at concentrations of 40and 20 µM. These results demonstrate that an elevated expression of inflammatorycytokines and TLR4 in cells stimulated with LPS, were simultaneously inhibitedby emodin. Emodin is therefore able to inhibit the LPS-induced expression of TLR4in order to downregulate TNFα and IL-6 synthesis in TECs, which may contributeto the protective effects of emodin in renal disease.

Suppression of lipopolysaccharide-induced upregulation of toll-like receptor 4 by emodin in mouse proximal tubular epithelial cells