국가연구개발성과

논문 (학술지)
The Anti-neuroinflammatory Activity of Tectorigenin Pretreatment via Downregulated NF-kappa B and ERK/JNK Pathways in BV-2 Microglial and Microglia Inactivation in Mice With Lipopolysaccharide

저자, 논문 구분, 저자, 학술지명, ISSN, SCI(SCIE포함) 구분, 학술지 출판 일자, 볼륨, 페이지, 학술지 임팩트 팩터, 학술대회명, 학술대회 개최국, 키워드 항목으로 구성된 논문 상세조회를 제공하고 데이터가 없는 항목에 대해서는 출력
등록번호 - SCI 구분
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 ※구분 : SCI(SCIE포함), 비SCI

SCI
저자명 (주·공동저자) Lim Hye-Sun; 임혜선; 정수진; 김유진; 김부여; 박건혁
※ 과제 참여정보와 일치하는 연구자 상세정보로 정확하지 않을 수 있습니다.
동일저자 논문보기
논문구분 국외전문학술지 학술지명 FRONTIERS IN PHARMACOLOGY
ISSN 1663-9812 학술지 출판일자 -
학술지 볼륨번호 9 논문페이지 0 ~ 13
학술지 임팩트팩터 3.831 기여율 100 %
DOI 10.3389/fphar.2018.00462
초록 The activation of microglia is decisively involved with the neurodegeneration observed in many neuroinflammatory pathologies, such as multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease. Tectorigenin (TEC) is an isoflavone isolated from various medicinal plants, such as Pueraria thunbergiana Benth, Belamcanda chinensis, and Iris unguicularis. In the present study, the neuroinflammatory effects of TEC were evaluated in both lipopolysaccharide (LPS)-treated BV-2 microglial and mouse models. TEC remarkably inhibited reactive oxygen species (ROS) generation. TEC also inhibits the production and expression of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-a (TNF-a), and interleukin-6 (IL-6) in LPS-stimulated BV-2 cells. In addition, TEC suppressed the LPS-induced activation of nuclear factor-kB (NF-kB), phosphorylation of extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) to regulate the inflammatory mediators, such as inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-a, and IL-6. These results indicate that TEC may inhibit neuronal inflammation through the downregulation of inflammatory mediators, including iNOS, COX-2, TNF-a, and IL-6 by suppressing NF-kB/ERK/JNKrelated signaling pathways. Furthermore, cotreatment with TEC and ERK inhibitor SCH772984 or JNK inhibitor SP600125 suppressed the overproduction of LPS-induced NO production in BV-2 cells. Consistent with the results of in vitro experiments, an LPSinduced brain inflammation mouse model, administration of TEC effectively decrease the levels of malondialdehyde, iNOS in hippocampus, and prevented increases in the levels of TNF-a and IL-6 in the serum. TEC showed marked attenuation of microglial activation. Finally, TEC inhibited protein expression of toll-like receptor 4 and myeloid differentiation factor 88 in LPS-activated BV-2 microglia and mouse models. Taken altogether, the cumulative findings suggested that TEC holds the potential to develop as a neuroprotective drug for the intervention of neuroinflammatory disorders.

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