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논문 기본 정보

자료유형
학술저널
저자정보
Heewon Song (Sejong University) Young Joo Lee (Sejong University)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.41 No.3
발행연도
2017.7
수록면
240 - 246 (7page)

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초록· 키워드

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Background: Korean Red Ginseng (KRG) is a traditional herbal medicine made by steaming and drying fresh ginseng. It strengthens the endocrine and immune systems to ameliorate various inflammatory responses. The cyclooxygenase-2 (COX-2)/prostaglandin E2 pathway has important implications for inflammation responses and tumorigenesis. Peroxisome proliferator-activated receptor gamma (PPARg) is a transcription factor that regulates not only adipogenesis and lipid homeostasis, but also angiogenesis and inflammatory responses.
Methods: The effects of the KRG on inhibition of hypoxia-induced COX-2 via PPARg in A549 cells were determined by luciferase assay,Western blot, and/or quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The antimigration and invasive effects of KRG were evaluated on A549 cells using migration and matrigel invasion assays.
Results and conclusion: We previously reported that hypoxia-induced COX-2 protein and mRNA levels were suppressed by KRG. This study examines the possibility of PPARg as a cellular target of KRG for the suppression of hypoxia-induced COX-2. PPARg protein levels and PPARg-responsive element (PPRE)-driven reporter activities were increased by KRG. Reduction of hypoxia-induced COX-2 by KRG was abolished by the PPARg inhibitor GW9662. In addition, the inhibition of PPARg abolished the effect of KRG on hypoxia-induced cell migration and invasion.
Discussion: Our results show that KRG inhibition of hypoxia-induced COX-2 expression and cell invasion is dependent on PPARg activation, supporting the therapeutic potential for suppression of inflammation under hypoxia. Further studies are required to demonstrate whether KRG activates directly PPARg and to identify the constituents responsible for this activity.

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ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References

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