In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng
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 s...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2017-01-01
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| Series: | Journal of Ginseng Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1226845315001335 |
| _version_ | 1831839122251055104 |
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| author | Muhammad Jahangir Hossen Yong Deog Hong Kwang-Soo Baek Sulgi Yoo Yo Han Hong Ji Hye Kim Jeong-Oog Lee Donghyun Kim Junseong Park Jae Youl Cho |
| author_facet | Muhammad Jahangir Hossen Yong Deog Hong Kwang-Soo Baek Sulgi Yoo Yo Han Hong Ji Hye Kim Jeong-Oog Lee Donghyun Kim Junseong Park Jae Youl Cho |
| author_sort | Muhammad Jahangir Hossen |
| collection | DOAJ |
| description | 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-β (TRIF), to measure the activation of nuclear factor (NF)-κB 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-β and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 and NF-κB (p50 and p65). This extract inhibited the upregulation of NF-κB-linked luciferase activity provoked by phorbal-12-myristate-13 acetate as well as MyD88, TRIF, and inhibitor of κB (IκBα) kinase (IKKβ), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-κB 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-κB and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K. |
| first_indexed | 2024-12-23T05:47:07Z |
| format | Article |
| id | doaj.art-51ea7b9876664b9bbabb1f7ad817aff1 |
| institution | Directory Open Access Journal |
| issn | 1226-8453 |
| language | English |
| last_indexed | 2024-12-23T05:47:07Z |
| publishDate | 2017-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Ginseng Research |
| spelling | doaj.art-51ea7b9876664b9bbabb1f7ad817aff12022-12-21T17:58:03ZengElsevierJournal of Ginseng Research1226-84532017-01-01411435110.1016/j.jgr.2015.12.009In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginsengMuhammad Jahangir Hossen0Yong Deog Hong1Kwang-Soo Baek2Sulgi Yoo3Yo Han Hong4Ji Hye Kim5Jeong-Oog Lee6Donghyun Kim7Junseong Park8Jae Youl Cho9Department of Genetic Engineering, Sungkyunkwan University, Suwon, KoreaHeritage Material Research Team, Amorepacific R&D Unit, Yongin, KoreaDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, KoreaDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, KoreaDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, KoreaDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, KoreaBio-inspired Aerospace Information Laboratory, Department of Aerospace Information Engineering, Konkuk University, Seoul, KoreaHeritage Material Research Team, Amorepacific R&D Unit, Yongin, KoreaHeritage Material Research Team, Amorepacific R&D Unit, Yongin, KoreaDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, KoreaBackground: 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-β (TRIF), to measure the activation of nuclear factor (NF)-κB 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-β and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 and NF-κB (p50 and p65). This extract inhibited the upregulation of NF-κB-linked luciferase activity provoked by phorbal-12-myristate-13 acetate as well as MyD88, TRIF, and inhibitor of κB (IκBα) kinase (IKKβ), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-κB 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-κB and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K.http://www.sciencedirect.com/science/article/pii/S1226845315001335anti-inflammatory activityantioxidative activityBIOGF1Kcompound KPanax ginseng |
| spellingShingle | Muhammad Jahangir Hossen Yong Deog Hong Kwang-Soo Baek Sulgi Yoo Yo Han Hong Ji Hye Kim Jeong-Oog Lee Donghyun Kim Junseong Park Jae Youl Cho In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng Journal of Ginseng Research anti-inflammatory activity antioxidative activity BIOGF1K compound K Panax ginseng |
| title | In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng |
| title_full | In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng |
| title_fullStr | In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng |
| title_full_unstemmed | In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng |
| title_short | In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng |
| title_sort | in vitro antioxidative and anti inflammatory effects of the compound k rich fraction biogf1k prepared from panax ginseng |
| topic | anti-inflammatory activity antioxidative activity BIOGF1K compound K Panax ginseng |
| url | http://www.sciencedirect.com/science/article/pii/S1226845315001335 |
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