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Ginsenoside Rd inhibits the expressions of iNOS and COX-2 by suppressing NF-κB in LPS-stimulated RAW264.7 cells and mouse liver

  • Kim, Dae Hyun (Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University) ;
  • Chung, Jae Heun (Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University) ;
  • Yoon, Ji Sung (Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University) ;
  • Ha, Young Mi (Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University) ;
  • Bae, Sungjin (Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University) ;
  • Lee, Eun Kyeong (Research Center, Dongnam Institute of Radiological and Medical Sciences) ;
  • Jung, Kyung Jin (Inhalation Toxicology Center, Korea Institute of Toxicology) ;
  • Kim, Min Sun (Department of Pharmacy, College of Pharmacy, Sunchon National University) ;
  • Kim, You Jung (Department of Dental Hygiene, Busan Women's College) ;
  • Kim, Mi Kyung (Longevity Life Science and Technology Institute, Pusan National University) ;
  • Chung, Hae Young (Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University)
  • Received : 2012.04.25
  • Accepted : 2012.10.06
  • Published : 2013.01.15

Abstract

Ginsenoside Rd is a primary constituent of the ginseng rhizome and has been shown to participate in the regulation of diabetes and in tumor formation. Reports also show that ginsenoside Rd exerts anti-oxidative effects by activating anti-oxidant enzymes. Treatment with ginsenoside Rd decreased nitric oxide and prostaglandin $E_2$ ($PGE_2$) in lipopolysaccharides (LPS)-challenged RAW264.7 cells and in ICR mouse livers (5 mg/kg LPS; LPS + ginsenoside Rd [2, 10, and 50 mg/kg]). Furthermore, these decreases were associated with the down-regulations of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 and of nuclear factor (NF)-${\kappa}B$ activity in vitro and in vivo. Our results indicate that ginsenoside Rd treatment decreases; 1) nitric oxide production (40% inhibition); 2) $PGE_2$ synthesis (69% to 93% inhibition); 3) NF-${\kappa}B$ activity; and 4) the NF-${\kappa}B$-regulated expressions of iNOS and COX-2. Taken together, our results suggest that the anti-inflammatory effects of ginsenoside Rd are due to the down-regulation of NF-${\kappa}B$ and the consequent expressional suppressions of iNOS and COX-2.

Keywords

References

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