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

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LI YING; Xiong Weijian; YANG JING; ZHONG JING; ZHANG LING; Zheng Jing; LIU HONG; ZHANG QI; Ouyang Xiaoqin; Lei Lei; Yu Xiao

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Journal: Iranian Journal of Kidney Diseases Year:2015 | Volume:9 | Issue:3 Page(s): 202-208

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Title

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

Author(s)

Keywords

emodin

toll-like receptor 2

lipopolysaccharides

inflammation

acute kidney injury

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-κ B 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 enzymelinked immunosorbent assay. The mRNA expression of TLR2, NF-κ B, 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-κ B and increased TNF-α , IL-1β , and IL-6 mRNA and protein levels. At doses of 20 μ M and 40μ M, emodin was able to inhibit LPS-induced TLR2, NF-κ B, 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-κ B signal pathway, which may contribute to the immune inflammation regulation of emodin in LPS-induced acute kidney injury.

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APA: Copy

LI, YING, Xiong, Weijian, YANG, JING, ZHONG, JING, ZHANG, LING, Zheng, Jing, LIU, HONG, ZHANG, QI, Ouyang, Xiaoqin, Lei, Lei, & Yu, Xiao. (2015). Attenuation of Inflammation by Emodin in Lipopolysaccharide-induced Acute Kidney Injury via Inhibition of Toll-like Receptor 2 Signal Pathway. IRANIAN JOURNAL OF KIDNEY DISEASES (IJKD), 9(3), 202-208. SID. https://sid.ir/paper/309535/en

Vancouver: Copy

LI YING, Xiong Weijian, YANG JING, ZHONG JING, ZHANG LING, Zheng Jing, LIU HONG, ZHANG QI, Ouyang Xiaoqin, Lei Lei, Yu Xiao. Attenuation of Inflammation by Emodin in Lipopolysaccharide-induced Acute Kidney Injury via Inhibition of Toll-like Receptor 2 Signal Pathway. IRANIAN JOURNAL OF KIDNEY DISEASES (IJKD)[Internet]. 2015;9(3):202-208. Available from: https://sid.ir/paper/309535/en

IEEE: Copy

YING LI, Weijian Xiong, JING YANG, JING ZHONG, LING ZHANG, Jing Zheng, HONG LIU, QI ZHANG, Xiaoqin Ouyang, Lei Lei, and Xiao Yu, “Attenuation of Inflammation by Emodin in Lipopolysaccharide-induced Acute Kidney Injury via Inhibition of Toll-like Receptor 2 Signal Pathway,” IRANIAN JOURNAL OF KIDNEY DISEASES (IJKD), vol. 9, no. 3, pp. 202–208, 2015, [Online]. Available: https://sid.ir/paper/309535/en

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