Toll-like receptor 4/nuclear factor-kappa B signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect
文献类型：期刊论文
| 作者 | Yang, Xinying2,3; Zhang, Guojian4; Tang, Xuelian2,5; Jiao, Jieying4; Kim, Sung Yeon6; Lee, Joo Young1; Zhu, Tianjiao4; Li, Dehai4; Yun, Yong Gab7; Gu, Qianqun4 |
| 刊名 | MOLECULAR AND CELLULAR BIOCHEMISTRY
 |
| 出版日期 | 2013-02 |
| 卷号 | 374期号:1-2页码:29-36 |
| 关键词 | ACTG-toxin H LPS TLR4/NF kappa B |
| ISSN号 | 0300-8177 |
| DOI | 10.1007/s11010-012-1502-9 |
| 文献子类 | Article |
| 英文摘要 | ACTG-toxin H (AH) originates from Alternaria sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1 beta, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-kappa B (NF kappa B) DNA-binding activity. Using transfection assay and measurement of an NF kappa B-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NF kappa B transcription activity in 293T cells. AH significantly blocked LPS-induced NF kappa B activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NF kappa B signaling pathway. |
| WOS关键词 | THERAPEUTIC TARGET ; NITRIC-OXIDE ; ACTIVATION ; INHIBITION ; KINASE ; CELLS ; COX-2 ; LIPOPOLYSACCHARIDE ; INFLAMMATION ; EXPRESSION |
| 资助项目 | Public Welfare & Safety Research Program through National Research Foundation (NRF)[00000000] ; Ministry of Education, Science and Technology[20120006545] ; Chinese National Natural Science Fund[30973627] ; Shandong Province of China[ZR2009CZ016] |
| WOS研究方向 | Cell Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:000312936500004 |
| 出版者 | SPRINGER |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/277758]  |
| 专题 | 新药研究国家重点实验室 中科院受体结构与功能重点实验室 |
| 通讯作者 | Park, Hyun |
| 作者单位 | 1.Gwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea; 2.Wonkwang Univ, Sch Med, Dept Infect Biol, Zoonosis Res Ctr, Iksan 570749, Jeonbuk, South Korea; 3.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Div Antitumor Pharmacol, Shanghai 201203, Peoples R China; 4.Ocean Univ China, Inst Marine Drugs & Food, Chinese Minist Educ, Key Lab Marine Drugs, Qingdao 266002, Peoples R China; 5.S China Agr Univ, Coll Anim Sci, Dept Aquaculture, Guangzhou 510642, Guangdong, Peoples R China; 6.Wonkwang Univ, Coll Pharm, Iksan 570749, Chonbuk, South Korea; 7.Wonkwang Univ, Dept Oriental Med, Iksan 570749, Chonbuk, South Korea |
| 推荐引用方式 GB/T 7714 | Yang, Xinying,Zhang, Guojian,Tang, Xuelian,et al. Toll-like receptor 4/nuclear factor-kappa B signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect[J]. MOLECULAR AND CELLULAR BIOCHEMISTRY,2013,374(1-2):29-36. |
| APA | Yang, Xinying.,Zhang, Guojian.,Tang, Xuelian.,Jiao, Jieying.,Kim, Sung Yeon.,...&Park, Hyun.(2013).Toll-like receptor 4/nuclear factor-kappa B signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect.MOLECULAR AND CELLULAR BIOCHEMISTRY,374(1-2),29-36. |
| MLA | Yang, Xinying,et al."Toll-like receptor 4/nuclear factor-kappa B signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect".MOLECULAR AND CELLULAR BIOCHEMISTRY 374.1-2(2013):29-36. |
入库方式： OAI收割
来源：上海药物研究所
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