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.

• Authors: Ying Li, Weijian Xiong, Jing Yang, Jin Zhong, Ling Zhang, Jing Zheng, Hong Liu, Qi Zhang, Xiaoqin Ouyang, Lei Lei, Xiao Yu
• Journal: Iranian journal of kidney diseases (Iran J Kidney Dis) Vol. 9 Issue 3 Pg. 202-8 (May 2015) ISSN: 1735-8604 [Electronic] Iran
• PMID: 25957424 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Interleukin-1beta
• Interleukin-6
• Lipopolysaccharides
• NF-kappa B
• Protein Kinase Inhibitors
• RNA, Messenger
• Toll-Like Receptor 2
• Tumor Necrosis Factor-alpha
• Emodin

Topics

• Acute Kidney Injury (chemically induced, drug therapy, immunology)
• Animals
• Cells, Cultured
• Emodin (pharmacology)
• Enzyme-Linked Immunosorbent Assay
• Epithelial Cells (drug effects)
• Inflammation (chemically induced, drug therapy, metabolism)
• Interleukin-1beta (metabolism)
• Interleukin-6 (metabolism)
• Lipopolysaccharides (toxicity)
• NF-kappa B (metabolism)
• Protein Kinase Inhibitors (pharmacology)
• RNA, Messenger (drug effects)
• Rats
• Signal Transduction (drug effects)
• Toll-Like Receptor 2 (metabolism)
• Tumor Necrosis Factor-alpha (metabolism)