Luteolin tetramethyl ether/Tetramethoxyluteolin/5,7,3',4'-Tetramethylluteolin/3',4',5,7-Tetramethyl-luteolin/5,7,3',4'-tetramethoxyflavone/Tetramethylluteolin/3',4',5,7-Tetramethoxyflavone/5,7,3'-trimethoxy 4'-hydroxyflavone
5,7,3',4'-Tetramethoxyflavone, one of the major polymethoxyflavones (PMFs) isolated from M. exotica, possesses various bioactivities, including anti-fungal, anti-malarial, anti-mycobacterial, and anti-inflammatory activities. 5,7,3',4'-Tetramethoxyflavone exhibits chondroprotective activity by targeting β-catenin signaling.
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Background: miR-29a, a downstream factor of Wnt/β-catenin signaling, promotes the activity of the Wnt/β-catenin signaling in a positive feedback loop. Our previous work showed that 5,7,3′,4′-tetramethoxyflavone (TMF), a major constituent from Murraya exotica L., exhibited chondroprotective activity by inhibiting the activity of Wnt/β-catenin signaling. Purpose: To investigate whether TMF showed the inhibitory effects on miR-29a/β-catenin signaling by up regulation of Foxo3a expression. Methods: Rat knee OA models were duplicated by using Hulth’s method. TMF (5 μg/mL and 20 μg/mL) was used for administration to cultured cells, which were isolated from the rat cartilages. Analysis of chondrocytes apoptosis, gene expression, and protein expression were conducted. In addition, miR-29a mimics and pcDNA3.1(+)-Foxo3a vector were used for transfection, luciferase reporter assay for detecting the activity of Wnt/β-catenin signaling, and co-immunoprecipitation for determining proteins interaction. Results: TMF down regulated miR-29a/β-catenin signaling activity and cleaved caspase-3 expression and up regulated Foxo3a expression in OA rat cartilages. In vitro, miR-29a mimics down regulated the expression of Foxo3a and up regulated the activity of Wnt/β-catenin signaling and cleaved caspase-3 expression. TMF ameliorated miR-29a/β-catenin-induced chondrocytes apoptosis by up regulation of Foxo3a expression. Conclusion: TMF exhibited chondroprotective activity by up regulating Foxo3a expression and subsequently inhibiting miR-29a/Wnt/β-catenin signaling activity.
Foxo3a; TMF; Wnt/β-catenin; chondrocytes apoptosis; miR-29a; osteoarthritis
TMF inhibits miR-29a/Wnt/β-catenin signaling through upregulating Foxo3a activity in osteoarthritis chondrocytes.
Huang X#1, Chen Z#1, Shi W1, Zhang R1, Li L1, Liu H1, Wu L1.
2019 Jun 19
Mast cells (MCs) are critical for allergic reactions but are also important in inflammatory processes. Stimulation by neuropeptides, such as substance P (SP) and neurotensin (NT), leads to release of preformed molecules stored in numerous MC secretory granules and newly synthesized proinflammatory mediators, including tumor necrosis factor, C-X-C motif chemokine ligand 8, and vascular endothelial growth factor. Here, we investigate the role of mammalian target of rapamycin (mTOR) signaling in the stimulation of cultured human LAD2 MCs by NT or SP, as well as the inhibitory effect of the natural flavonoids 3′,4′,5,7-tetrahydroxyflavone (luteolin) and its novel structural analog 3′,4′,5,7-tetramethoxyflavone (methoxyluteolin). Stimulation by NT (10 μM) or SP (1 μM) increases (P < 0.0001) gene expression (after 6 hours) and release (after 24 hours) of tumor necrosis factor, C-X-C motif chemokine ligand 8, and vascular endothelial growth factor. This occurs via activation of both mTOR complexes, as denoted by the increased phosphorylated (p) protein levels (P < 0.0001) of the downstream mTORC1 substrate pp70S6KThr389 and mTORC2 component pmTORSer2448. Pretreatment of human MCs using the mTORC1 inhibitor rapamycin, the mTORC1/mTORC2 inhibitor Torin1, or the two flavonoids decreases both gene expression and release (P < 0.0001) of all three mediators. Methoxyluteolin is a more potent human MC inhibitor than luteolin or Torin1, implicating other MC protein targets in addition to the mTOR complex. These findings indicate that mTOR is partially involved in the neuropeptide stimulation of MCs, but the novel flavonoid methoxyluteolin inhibits the response entirely, suggesting that it may be developed for treatment of allergic and inflammatory diseases. Copyright © 2017 by The American Society for Pharmacology and Experimental Therapeutics.
Methoxyluteolin Inhibits Neuropeptide-stimulated Proinflammatory Mediator Release via mTOR Activation from Human Mast Cells.
Patel AB1, Theoharides TC2.
Osteoarthritis (OA) is a progressive joint disorder, which remains the leading cause of chronic disability in aged people. This study is the first report which demonstrates the cartilage protective effect of 5,7,3′,4′-tetramethoxyflavone (TMF) by decreasing the concentration of IL-1β, TNF-α and PGE2 in the knee synovial fluid in OA rat models in vivo. In vitro, after induced by PGE2, the apoptosis rate of chondrocytes was significantly increased. In addition, PGE2 increased the expression of cAMP/PKA signaling pathway in chondrocytes, stabilized and accumulated β-catenin, and activated the expression of β-catenin signaling pathway. These activities were counteracted by TMF dose-dependently. Collectively, TMF is a potential compound with chondroprotective activity by inhibiting both EP/cAMP/PKA signaling pathway and β-catenin signaling pathway.
Copyright © 2014 Elsevier Inc. All rights reserved.
5,7,3′,4′-Tetramethoxyflavone; Chondrocytes; Osteoarthritis; PGE(2); β-Catenin
5,7,3',4'-Tetramethoxyflavone exhibits chondroprotective activity by targeting β-catenin signaling in vivo and in vitro.
Wu L1, Liu H2, Li L2, Liu H2, Yang K2, Liu Z2, Huang H2.
2014 Sep 26;