Modulation of Suppressive Activity of Lipopolysaccharide-Induced Nitric Oxide Production by Glycosidation of Flavonoids

  • Kwon, Yong-Soo (College of Pharmacy, Kangwon National University) ;
  • Kim, Sung-Soo (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Sohn, Soon-Joo (College of Pharmacy, Kangwon National University) ;
  • Kong, Pil-Jae (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Cheong, Il-Young (Department of Anesthesiology, College of Medicine, Kangwon National University) ;
  • Kim, Chang-Min (College of Pharmacy, Kangwon National University) ;
  • Chun, Wan-Joo (Department of Pharmacology, College of Medicine, Kangwon National University)
  • Published : 2004.07.01

Abstract

Flavonoids have been demonstrated to exhibit a wide range of biological activities including anti-inflammatory and neuroprotective actions. Although a significant amount of flavonoids has been identified to be present as glycosides in medicinal plants, determinations of the biological activities of flavonoids were mainly carried out with aglycones of flavonoids. Therefore, the exact role of the glycosidation of flavonoid aglycones needs to be established. In an attempt to understand the possible role of glycosidation on the modulation of the biological activities of flavonoids, diverse glycosides of kaempferol, quercetin, and aromadendrin were examined in terms of their anti-inflammatory activity determined with the suppression of lipopolysaccharide (LPS)-induced nitric oxide (NO) production in BV2 microglial cells. The results indicated that glycosidation of aglycones attenuated the suppressive activity of aglycones on LPS-induced NO production. Although attenuated, some of glycosides, depending on the position and degree of glycosidation, maintained the inhibitory capability of LPS-induced NO production. These findings suggest that glycosidation of flavonoid aglycones should be considered as an important modulator of the biological activities of flavonoids.

Keywords

References

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