Identification of the Constituents for Nrf2 Activation and NF-${\kappa}B$ Suppression in Dangguisoo-san

  • Kim, Kyun-Ha (School of Korean Medicine, Pusan National University) ;
  • Jeong, Ja-Haeng (School of Korean Medicine, Pusan National University) ;
  • Jeong, Han-Sol (School of Korean Medicine, Pusan National University) ;
  • Ha, Ki-Tae (School of Korean Medicine, Pusan National University) ;
  • Joo, Myung-Soo (School of Korean Medicine, Pusan National University)
  • Received : 2012.04.14
  • Accepted : 2012.06.16
  • Published : 2012.06.25

Abstract

Previously, we showed that Dangguisoo-san (DGSS), an herbal formula that has been traditionally used for the treatment of blood stagnation, is also applicable for inflammatory lung diseases. Activation of Nrf2, an anti-inflammatory transcription factor, and suppression of NF-${\kappa}B$, a pro-inflammatory transcription factor, were suggested as an underlying mechanism. However, the constituents responsible for these activities remain unidentified. To this end, we prepared the water extracts of the 9 constituents of DGSS and tested for their effect on Nrf2 by using an Nrf2-Luciferase reporter cell line and western blot analysis. Results show that Carthamus tinctorius L.(CT), one of the 9 constituents of DGSS, strongly activated Nrf2. Similarly, when measured the effect of the 9 constituents on NF-${\kappa}B$ by using an NF-${\kappa}B$-Luciferase reporter cell line and western blotting for nuclear p65, indicative of activated NF-${\kappa}B$, most constituents were capable of suppressing NF-${\kappa}B$ in various degrees. However, CT and Cyperus rotundus L. (CR) strongly suppressed NF-${\kappa}B$ activity elicited by LPS. Of note, CT activated Nrf2 and suppressed NF-${\kappa}B$ strongly as well. Our results contributes to corroborating the anti-inflammatory effects of DGSS by identifying CT and CR as two major herbs responsible for activating Nrf2 and suppressing NF-${\kappa}B$. These results suggest that CT and CR represent some of the effects of DGSS in the regulation of inflammation.

Keywords

References

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