Attenuation of Inflammation by Emodin in Lipopolysaccharide-induced Acute Kidney Injury via Inhibition of Toll-like Receptor 2 Signal Pathway

Abstract

Introduction. Emodin, an anthraquinone derivative from the Chinese herb Radix et Rhizoma Rhe, has been reported to possess anti-inflammatory property in vivo and in vitro. However, the effect of emodin on inflammation in lipopolysaccharide (LPS)-induced acute kidney injury as an immunomodulator has yet to be determined. This study aimed to investigate whether emodin had protective effects against LPS-induced acute kidney injury by inhibiting toll-like receptor 2 (TLR2) signal pathway in normal rat kidney epithelial cells (NRK-52E).

Materials and Methods. The NRK-52E cells were incubated with LPS with and without the indicated concentrations of emodin for 24 hours. The TLR2 and NF-κB protein level was detected by Western blot method. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 protein levels were measured using an enzyme-linked immunosorbent assay. The mRNA expression of TLR2, NF-κB, TNF-α, IL-1β, and IL-6 was detected using a real-time polymersase chain reaction.

Results. A concentration of 10² ng/mL of LPS significantly upregulated mRNA and protein levels of TLR2 and NF-κB and increased TNF-α, IL-1β, and IL-6 mRNA and protein levels. At doses of 20 µM and 40 µM, emodin was able to inhibit LPS-induced TLR2, NF-κB, TNF-α, IL-1β and IL-6 mRNA and protein expressions in cultured NRK-52E cells.

Conclusions. These results demonstrate that an elevated expression of inflammatory cytokines and TLR2 in cells stimulated by LPS were simultaneously inhibited by emodin. Therefore, emodin attenuates the inflammation by inhibiting TLR2-mediated NF-κB signal pathway, which may contribute to the immune inflammation regulation of emodin in LPS-induced acute kidney injury.