상위피인용논문
- 조회411
Mi-Sun Kim 1, Sang-Hyun Kim 1,*
1Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu, 700-422, Korea.
*Corresponding author: correspondence to Sang-Hyun Kim
Abstract
Astragalin (kaempferol-3-O-glucoside), a newly found flavonoid from leaves of persimmon or Rosa agrestis, is known to have antiatopic dermatitis and antioxidant activity. However, the effect of astragalin on the inflammatory response is not well defined. Nitric oxide (NO) produced from the activated macrophages is well known as a mediator of inflammation. Transcription factor (NF)-κB mediates the inducible expression of a variety of genes involved in immune and inflammatory responses including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and cytokines/chemokines. In the present study, we examined the inhibitory effects of astragalin on the lipopolysaccharide (LPS)-induced inflammatory mediators. Astragalin significantly reduced LPS-induced expression of iNOS, COX-2 and cytokines/chemokines, and production of NO in J774A.1 mouse macrophages. Astragalin inhibited LPSinduced activation of NF-κB as indicated by inhibition of degradation of IκBα, nuclear translocation of NF-κB, and NF-κB dependent gene reporter assay. The inhibitory effects of astragalin on the inflammatory mediators are comparable with quercetin, a well known flavonoid possessing antioxidant and anti-inflammatory activity. Using the mouse peritoneal macrophages, we confirmed the inhibitory effect of astragalin on NO production and NF-κB activation. Taken together, our results indicate that astragalin inhibits expression of proinflammatory mediators through the inhibition of NF-κB in macrophages.
논문정보
- Research article
- 2011년 12월 (BRIC 등록일 2024-03-05)
- 국내 연구진
- 의약학 > 약리의학
- 120회 이상 인용된 논문
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