Anti-inflammatory Effect of the Hot Water Extract from Sasa quelpaertensis Leaves

  • Hwang, Joon-Ho (Technology Innovation Center for Life Science, Cheju National University) ;
  • Choi, Soo-Yoon (Technology Innovation Center for Life Science, Cheju National University) ;
  • Ko, Hee-Chul (Technology Innovation Center for Life Science, Cheju National University) ;
  • Jang, Mi-Gyeong (Technology Innovation Center for Life Science, Cheju National University) ;
  • Jin, Young-Jon (Department of Life Science, Cheju National University) ;
  • Kang, Seong-Il (Department of Life Science, Cheju National University) ;
  • Park, Ji-Gweon (Technology Innovation Center for Life Science, Cheju National University) ;
  • Chung, Wan-Seok (Technology Innovation Center for Life Science, Cheju National University) ;
  • Kim, Se-Jae (Department of Life Science, Cheju National University)
  • Published : 2007.10.31

Abstract

Bamboo grass, Sasa quelpaertensis, is a native plant to Jeju Island, Korea. The leaves of Sasa plants are widely used in traditional Korean medicine to treat inflammation-related diseases. We investigated the effect of hot water extract from Sasa quelpaertensis leaves (HWE-SQ) on nitric oxide (NO) production and nuclear $factor-{\kappa}B\;(NF-{\kappa}B)$ activation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. HWE-SQ inhibited LPS-induced NO production and inducible NO synthase (iNOS) protein expression in a dose-dependent manner. Reporter gene assays indicated that HWE-SQ decreases LPS-induced $NF-{\kappa}B$ transcriptional activation. However, HWE-SQ did not affect the phosphorylation and degradation of inhibitory ${\kappa}B{\alpha}\;(1{\kappa}B{\alpha})$. HWE-SQ also directly inhibited iNOS enzyme activity in a dose-dependent manner. These results suggest that HWE-SQ suppresses NO synthesis in macrophages by attenuating $NF-{\kappa}B-mediated$ iNOS protein expression and inhibiting iNOS enzymatic activity, thereby implicating a mechanism by which HWE-SQ is able to ameliorate inflammation-related diseases by limiting excessive or prolonged NO production in pathological events.

Keywords

References

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