플라보노이드 루테올린의 lippopolysacharide로 유도한 type 1 interferon 억제 효과

Type I interferons (IFNs) are critical mediators of the innate immune system to defend viral infection. Interferon regulatory factor (IRF) and signal transducer and activator of transcription (STAT) play critical roles in type I IFN production in response to viral infection. Luteolin is natural poly...

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Published in동의생리병리학회지 Vol. 23; no. 5; pp. 986 - 992
Main Authors 정원석(Won Seok Jung), 배기상(Gi Sang Bae), 조창래(Chang Re Cho), 박경철(Kyoung Chel Park), 구본순(Bon Soon Koo), 김민선(Min Sun Kim), 함경완(Kyung Wan Ham), 조범연(Beom Yeon Jo), 조길환(Gil Hwan Cho), 서상완(Sang Wan Seo), 이시우(Siwoo Lee), 송호준(Ho Joon Song), 박성주(Sung Joo Park)
Format Journal Article
LanguageKorean
Published 한의병리학회 2009
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ISSN1738-7698
2288-2529
2283-2529

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Summary:Type I interferons (IFNs) are critical mediators of the innate immune system to defend viral infection. Interferon regulatory factor (IRF) and signal transducer and activator of transcription (STAT) play critical roles in type I IFN production in response to viral infection. Luteolin is natural polyphenolic compounds that have anti-inflammatory, cytoprotective and anti-carcinogenic effects. However, the mechanism of action and impact of luteolin on innate immunity is still unknown. In this study, we examined the effects of luteolin on the lipopolysacchride (LPS)-induced inflammatory responses. Luteolin inhibited Type I IFNs expression of mRNA and increased interleukin(IL)-10 expression of mRNA. Next, we examined the protective effects of IL-10 using IL-10 neutralizing antibody (IL-10NA). Blockade of IL-10 action didn't cause a significant reduction of Type I IFNs than LPS-induced luteolin pretreatment. Pretreatment of luteolin inhibited the level of IRF-1, and IRF-7 mRNA and the nuclear translocation of IRF-3. Also, luteolin reduced the activation of STAT - 1, 3. Theses results suggest that luteolin inhibits LPS-induced the production of Type I IFNS by both IRFs and STATs not IL-10 and may be a beneficial drug for the treatment of inflammatory disease.
Bibliography:KISTI1.1003/JNL.JAKO200908856862755
G704-000534.2009.23.5.027
ISSN:1738-7698
2288-2529
2283-2529