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Inhibitory Effect of Alopecurus aequalis Sobol Ethanol Extracts on LPS-induced Inflammatory Response in RAW 264.7 Cells

LPS로 유도한 RAW 264.7 세포의 염증반응에서 뚝새풀 에탄올 추출물의 억제 효과

  • Jung, Ho Kyung (Jeollanamdo Development Institute of Traditional Korean Medicine) ;
  • Kang, Byoung Man (Jeollanamdo Development Institute of Traditional Korean Medicine) ;
  • Jang, Ji Hun (Jeollanamdo Development Institute of Traditional Korean Medicine) ;
  • Ahn, Byung Kwan (Jeollanamdo Development Institute of Traditional Korean Medicine) ;
  • Yeo, Jun Hwan (Jeollanamdo Development Institute of Traditional Korean Medicine) ;
  • Jung, Won Seok (Jeollanamdo Development Institute of Traditional Korean Medicine) ;
  • Cho, Jung Hee (Jeollanamdo Development Institute of Traditional Korean Medicine) ;
  • Kuk, Yong In (Department of Development in Resource Plants, College of Life Science and Natural Resources, Sunchon National University) ;
  • Hyun, Kyu Hwan (Department of Development in Resource Plants, College of Life Science and Natural Resources, Sunchon National University) ;
  • Cho, Hyun Woo (Jeollanamdo Development Institute of Traditional Korean Medicine)
  • Received : 2013.12.03
  • Accepted : 2014.02.14
  • Published : 2014.04.30

Abstract

In the present study, we investigated the anti-inflammatory effects by Alopecurus aequalis Sobol on the lipopolysaccharide (LPS)-induced nitric oxide (NO) production by RAW 264.7 cell line. Consistent with these observations, DS reduced the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein levels in a concentration-dependent manner. In addition, the release of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) were also reduced by DS. Moreover, LPS increased expression phosphorylation of $I{\kappa}B{\alpha}$, but DS showed inhibitory effect by reducing LPS-inducible p-$I{\kappa}B{\alpha}$ expression level. These results suggest that the down regulation of iNOS, COX-2, TNF-${\alpha}$, and IL-6 expression by DS are achieved by the downregulation of NF-${\kappa}B$ activity, a transcription factor necessary for pro-inflammatory mediators, and that is also responsible for its anti-inflammatory effects.

Keywords

References

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