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논문 기본 정보

자료유형
학술저널
저자정보
Yanyan Yang (Sungkyunkwan University) Jongsung Lee (Eulji University) Man Hee Rhee (Kyungpook National University) Tao Yu (Sungkyunkwan University) Kwang-Soo Baek (Sungkyunkwan University) Nak Yoon Sung (Sungkyunkwan University) Yong Kim (Sungkyunkwan University) Keejung Yoon (Sungkyunkwan University) Ji Hye Kim (Sungkyunkwan University) Yi-Seong Kwak (Ginseng Corporation Central Research Institute) Sungyoul Hong (Sungkyunkwan University) Jong-Hoon Kim (Chonbuk National University) Jae Youl Cho (Sungkyunkwan University)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.39 No.1
발행연도
2015.1
수록면
61 - 68 (8page)

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초록· 키워드

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Background: Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and antiinflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activity.
Methods: We investigated the anti-inflammatory mechanisms of the protopanaxadiol saponin fraction (PPD-SF) of KRG using in vitro and in vivo inflammatory models.
Results: PPD-SF dose-dependently diminished the release of inflammatory mediators [nitric oxide (NO), tumor necrosis factor-α, and prostaglandin E₂], and downregulated the mRNA expression of their corresponding genes (inducible NO synthase, tumor necrosis factor-α, and cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression of these events appeared to be regulated by a blockade of p38, c-Jun N-terminal kinase (JNK), and TANK (TRAF family member-associated NF-kappa-B activator)-binding kinase 1 (TBK1), which are linked to the activation of activating transcription factor 2 (ATF2) and interferon regulatory transcription factor 3 (IRF3). Moreover, this fraction also ameliorated HCl/ethanol/-induced gastritis via suppression of phospho-JNK2 levels.
Conclusion: These results strongly suggest that the anti-inflammatory action of PPD-SF could be mediated by a reduction in the activation of p38-, JNK2-, and TANK-binding-kinase-1-linked pathways and their corresponding transcription factors (ATF2 and IRF3).

목차

abstract
1. Introduction
2. Materials and methods
3. Results and discussion
References

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