title: Luteolin inhibits inflammatory responses via p38/MK2/TTP-mediated mRNA stability.
abstract: Luteolin (Lut) is a common dietary flavonoid present in Chinese herbal medicines that has been reported to have important anti-inflammatory properties. The purposes of this study were to observe the inhibition of lipopolysaccharide (LPS)-induced inflammatory responses in bone marrow macrophages (BMM) by Lut, and to examine whether this inhibition involves p38/MK2/TTP-mediated mRNA stability. Lut suppressed the production of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in a dose-dependent manner according to enzyme-linked immunosorbent assay (ELISA) analysis. Lut also shortened the half-lives of the TNF-α and IL-6 mRNAs according to real-time PCR analysis. Western blots were performed to assess the activation of p38 and MK2 as well as the expression of TTP. The results indicated that Lut inhibited p38 and MK2 phosphorylation while promoting TTP expression. These results suggest that the anti-inflammatory effects of Lut are partially mediated through p38/MK2/TTP-regulated mRNA stability.
authors.affiliation: Institute of Cardiovascular Disease Research, Xuzhou Medical College, 84 West Huaihai Road, Xuzhou 221002, Jiangsu, China.
authors.forename: Wanling
authors.initials: W
authors.lastname: Wu
authors.forename: Dongye
authors.initials: D
authors.lastname: Li
authors.forename: Yu
authors.initials: Y
authors.lastname: Zong
authors.forename: Hong
authors.initials: H
authors.lastname: Zhu
authors.forename: Defeng
authors.initials: D
authors.lastname: Pan
authors.forename: Tongda
authors.initials: T
authors.lastname: Xu
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Tingting
authors.initials: T
authors.lastname: Wang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000378:metabolism / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000737:chemistry / Q000494:pharmacology*; D004365:Drugs, Chinese Herbal / Q000378:metabolism / Q000494:pharmacology; D004789:Enzyme Activation / Q000187:drug effects; D005260:Female; D005269:Femur; D015850:Interleukin-6 / Q000096:biosynthesis; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D047311:Luteolin / Q000737:chemistry / Q000494:pharmacology*; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D008297:Male; D010766:Phosphorylation / Q000187:drug effects; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D020871:RNA Stability / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D013977:Tibia; D051816:Tristetraprolin / Q000096:biosynthesis* / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D000099190:MAP-Kinase-Activated Kinase 2
chemical_list: D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D004365:Drugs, Chinese Herbal; D015850:Interleukin-6; D047908:Intracellular Signaling Peptides and Proteins; D047311:Luteolin; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger; D051816:Tristetraprolin; D014409:Tumor Necrosis Factor-alpha; D048051:p38 Mitogen-Activated Protein Kinases; D000099190:MAP-Kinase-Activated Kinase 2