KMID : 0352720170410010043
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Journal of Ginseng Research 2017 Volume.41 No. 1 p.43 ~ p.51
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In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng
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Hossen Muhammad Jahangir
Hong Yong-Deog Baek Kwang-Soo Yoo Sul-Gi Hong Yo-Han Kim Ji-Hye Lee Jeong-Oog Kim Dong-Hyun Park Jun-Seong Cho Jae-Youl
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Abstract
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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 anti-inflammatory 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-¥â (TRIF), to measure the activation of nuclear factor (NF)-¥êB and interferon regulatory factor 3 (IRF3).
Results: BIOGF1K suppressed lipopolysaccharide-triggered NO release in macrophages as well as DPPH-induced electron-donating activity. It also blocked lipopolysaccharide-induced mRNA levels of interferon-¥â and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 and NF-¥êB (p50 and p65). This extract inhibited the upregulation of NF-¥êB-linked luciferase activity provoked by phorbal-12-myristate-13 acetate as well as MyD88, TRIF, and inhibitor of ¥êB (I¥êB¥á) kinase (IKK¥â), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-¥êB pathway by blocking IKK¥â and the IRF3 pathway by inhibiting TBK1, according to reporter gene assays, immunoblotting analysis, and an AKT/IKK¥â/TBK1 overexpression strategy.
Conclusion: Overall, our data suggest that the suppression of IKK¥â and TBK1, which mediate transcriptional regulation of NF-¥êB and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K.
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KEYWORD
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anti-inflammatory activity, antioxidative activity, BIOGF1K, compound K, Panax ginseng
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