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논문 기본 정보

자료유형
학술저널
저자정보
Ye Lin (School of Pharmacy Changzhou University Changzhou ChinaDepartment of Pharmacology Yong Loo Lin Scho) Xin Yang (Food Science and Technology Program Department of Chemistry Faculty of Science National University) Wu Zhi-yuan (Department of Pharmacology Yong Loo Lin School of Medicine National University of Singapore Singapo) Sun Hai-jian (Department of Pharmacology Yong Loo Lin School of Medicine National University of Singapore Singapo) Huang De-jian (Food Science and Technology Program Department of Chemistry Faculty of Science National University) Sun Zhi-qin (Changzhou Second People's Hospital Changzhou ChinaSchool of Pharmacy Changzhou University Changzhou)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제32권 제1호
발행연도
2022.1
수록면
15 - 26 (12page)
DOI
10.4014/jmb.2104.04027

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초록· 키워드

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Luteolin is a common dietary flavone possessing potent anti-inflammatory activities. However, when administrated in vivo, luteolin becomes methylated by catechol-O-methyltransferases (COMT) owing to the catechol ring in the chemical structure, which largely diminishes its anti-inflammatory effect. In this study, we made a modification on luteolin, named LUA, which was generated by the chemical reaction between luteolin and 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH). Without a catechol ring in the chemical structure, this new flavone could escape from the COMTcatalyzed methylation, thus affording the potential to exert its functions in the original form when administrated in the organism. Moreover, an LPS-stimulated RAW cell model was applied to detect the anti-inflammatory properties. LUA showed much more superior inhibitory effect on LPS-induced production of NO than diosmetin (a major methylated form of luteolin) and significantly suppressed upregulation of iNOS and COX-2 in macrophages. LUA treatment dramatically reduced LPSstimulated reactive oxygen species (ROS) and mRNA levels of pro-inflammatory mediators such as IL-1β, IL-6, IL-8 and IFN-β. Furthermore, LUA significantly reduced the phosphorylation of JNK and p38 without affecting that of ERK. LUA also inhibited the activation of NF-κB through suppression of p65 phosphorylation and nuclear translocation.

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