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Innate Immunity Activation and Anti-Inflammation Effects of Evodia Rutaecarpine Water Extract

오수유 물 추출물의 선천 면역 활성과 염증 억제 효과

  • Jeong, So-Mi (Dept. of Clinical Korean Medicine, Graduate School, Kyung Hee University) ;
  • Lee, Jin-Moo (Dept. of Clinical Korean Medicine, Graduate School, Kyung Hee University) ;
  • Lee, Chang-Hoon (Dept. of Clinical Korean Medicine, Graduate School, Kyung Hee University) ;
  • Hwang, Deok-Sang (Dept. of Clinical Korean Medicine, Graduate School, Kyung Hee University) ;
  • Jang, Jun-Bock (Dept. of Clinical Korean Medicine, Graduate School, Kyung Hee University)
  • 정소미 (경희대학교 대학원 임상한의학과) ;
  • 이진무 (경희대학교 대학원 임상한의학과) ;
  • 이창훈 (경희대학교 대학원 임상한의학과) ;
  • 황덕상 (경희대학교 대학원 임상한의학과) ;
  • 장준복 (경희대학교 대학원 임상한의학과)
  • Received : 2021.04.15
  • Accepted : 2021.05.28
  • Published : 2021.05.28

Abstract

Objectives: This study was designed to examine immuno-modulatory effects of Evodia Rutaecarpine by activating innate immune system and inhibiting inflammation. Methods: First, Cell cytotoxicity was examined with 4T1 breast carcinoma and TG-induced macrophage. To investigate activating innate immune system of Evodiamine Rutacarpine Extract (ERE) on macrophage, we tested tumor necrosis factor-alpha (TNF-α), interleukin-12 (IL-12), and interleukin-6 (IL-6). In addition, TNF-α and nitric oxide (NO) induced by lipopolysaccharide (LPS) were measured after treating with ERE to observe innate immune modulating effect of ERE on RAW 264.7 cell. Also, mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) were examined by western blot analysis. Results: In cytotoxicity analysis, ERE significantly affected tumor cell growth above specific concentration. Also, ERE significantly affected macrophage growth above specific concetration. As compared with the control group, the production of TNF-α, IL-12 and IL-6 were increased in TG-induced macrophage. As compared with the control group, TNF-α and IL-6 were significantly up-regulated in RAW 264.7 cell. The expression of TNF-α and NO induced by LPS after treating ERE was significantly decreased compared with control group. In addition, We observed ERE inhibited the phosphorylation levels of p-extracellular signal-regulated kinase (p-ERK), p-Jun N-terminal kinase (p-JNK), and p-p38 in western blotting by treating ERE on RAW 264.7 cell. Conclusions: ERE seems to have considerable impact on the anti-cancer effect by activation of innate immune system and inflammation control.

Keywords

References

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