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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2017.1
- 수록면
- 43 - 51 (9page)
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초록· 키워드
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Background: BIOGF1K, a compound K-rich fraction prepared from the root of Panax ginseng, is widely used for cosmetic purposes in Korea. We investigated the functional mechanisms of the antiinflammatory and antioxidative activities of BIOGF1K by discovering target enzymes through various molecular studies.
Methods: We explored the inhibitory mechanisms of BIOGF1K using lipopolysaccharide-mediated inflammatory responses, reporter gene assays involving overexpression of toll-like receptor adaptor molecules, and immunoblotting analysis. We used the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay to measure the antioxidative activity. We cotransfected adaptor molecules, including the myeloid differentiation primary response gene 88 (MyD88) and Toll/interleukin-receptor domain containing adaptor molecule-inducing interferon-β (TRIF), to measure the activation of nuclear factor (NF)-kB and interferon regulatory factor 3 (IRF3).
Results: BIOGF1K suppressed lipopolysaccharide-triggered NO release in macrophages as well as DPPHinduced electron-donating activity. It also blocked lipopolysaccharide-induced mRNA levels of interferon-β and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 andNF-kB (p50 and p65). This extract inhibited the upregulation ofNF-kB-linked luciferase activity provoked by phorbal-12-myristate-13 acetate aswell asMyD88, TRIF, and inhibitor of kB (IkBα) kinase(IKKβ), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-kB pathway by blocking IKKβ and the IRF3 pathway by inhibiting TBK1, according to reporter gene assays, immunoblotting analysis, and an AKT/IKKβ/TBK1 overexpression strategy.
Conclusion: Overall, our data suggest that the suppression of IKKβ and TBK1, which mediate transcriptional regulation of NF-kB and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K.
Methods: We explored the inhibitory mechanisms of BIOGF1K using lipopolysaccharide-mediated inflammatory responses, reporter gene assays involving overexpression of toll-like receptor adaptor molecules, and immunoblotting analysis. We used the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay to measure the antioxidative activity. We cotransfected adaptor molecules, including the myeloid differentiation primary response gene 88 (MyD88) and Toll/interleukin-receptor domain containing adaptor molecule-inducing interferon-β (TRIF), to measure the activation of nuclear factor (NF)-kB and interferon regulatory factor 3 (IRF3).
Results: BIOGF1K suppressed lipopolysaccharide-triggered NO release in macrophages as well as DPPHinduced electron-donating activity. It also blocked lipopolysaccharide-induced mRNA levels of interferon-β and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 andNF-kB (p50 and p65). This extract inhibited the upregulation ofNF-kB-linked luciferase activity provoked by phorbal-12-myristate-13 acetate aswell asMyD88, TRIF, and inhibitor of kB (IkBα) kinase(IKKβ), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-kB pathway by blocking IKKβ and the IRF3 pathway by inhibiting TBK1, according to reporter gene assays, immunoblotting analysis, and an AKT/IKKβ/TBK1 overexpression strategy.
Conclusion: Overall, our data suggest that the suppression of IKKβ and TBK1, which mediate transcriptional regulation of NF-kB and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References
참고문헌 (57)
참고문헌 신청
[학술지(정기간행물)] - Steel HC / 2013 / Overview of communityacquired pneumonia and the role of inflammatory mechanisms in the immunopathogenesis of severe pneumococcal disease / Mediators Inflamm 2013 : 490346 ~
[학술지(정기간행물)] - Hiraiwa K / 2013 / Contribution of lung macrophages to the inflammatory responses induced by exposure to air pollutants / Mediators Inflamm 2013 : 619523 ~
[학술지(정기간행물)] - Hossen MJ / 2015 / In vivo and in vitro anti-inflammatory activities of Persicaria chinensis methanolic extract targeting Src/Syk/NF-kappaB / J Ethnopharmacol 159 : 9 ~ 16
[학술지(정기간행물)] - Yang RC / 2014 / Davallia bilabiata inhibits TNF-a-induced adhesion molecules and chemokines by suppressing IKK/NF-kappa B pathway in vascular endothelial cells / Am J Chin Med 42 : 1411 ~ 1429
[학술지(정기간행물)] - 원진배 / 2013 / Effect of Codonopsis lanceolata with Steamed and Fermented Process on Scopolamine-Induced Memory Impairment in Mice / Biomolecules & Therapeutics 21 (5) : 405 ~ 410
[학술지(정기간행물)] - Hiraiwa K / 2013 / Contribution of lung macrophages to the inflammatory responses induced by exposure to air pollutants / Mediators Inflamm 2013 : 619523 ~
[학술지(정기간행물)] - Hossen MJ / 2015 / In vivo and in vitro anti-inflammatory activities of Persicaria chinensis methanolic extract targeting Src/Syk/NF-kappaB / J Ethnopharmacol 159 : 9 ~ 16
[학술지(정기간행물)] - Yang RC / 2014 / Davallia bilabiata inhibits TNF-a-induced adhesion molecules and chemokines by suppressing IKK/NF-kappa B pathway in vascular endothelial cells / Am J Chin Med 42 : 1411 ~ 1429
[학술지(정기간행물)] - 원진배 / 2013 / Effect of Codonopsis lanceolata with Steamed and Fermented Process on Scopolamine-Induced Memory Impairment in Mice / Biomolecules & Therapeutics 21 (5) : 405 ~ 410
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UCI(KEPA) : I410-ECN-0101-2018-524-001598678