About: Therapeutic Effects of Tryptanthrin and Tryptanthrin-6-Oxime in Models of Rheumatoid Arthritis

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About: Therapeutic Effects of Tryptanthrin and Tryptanthrin-6-Oxime in Models of Rheumatoid Arthritis Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Therapeutic Effects of Tryptanthrin and Tryptanthrin-6-Oxime in Models of Rheumatoid Arthritis
Creator	Grabiec, Aleksander Salomone, Salvatore Hammaker, Deepa Karonitsch, Thomas Khlebnikov, Andrei Kirpotina, Liliya Kuhs, Amanda Quinn, Mark Schepetkin, Igor
Source	PMC
abstract	Rheumatoid arthritis (RA) is a chronic autoimmune disease involving joint and bone damage that is mediated in part by proteases and cytokines produced by synovial macrophages and fibroblast-like synoviocytes (FLS). Although current biological therapeutic strategies for RA have been effective in many cases, new classes of therapeutics are needed. We investigated anti-inflammatory properties of the natural alkaloid tryptanthrin (TRYP) and its synthetic derivative tryptanthrin-6-oxime (TRYP-Ox). Both TRYP and TRYP-Ox inhibited matrix metalloproteinase (MMP)-3 gene expression in interleukin (IL)-1β-stimulated primary human FLS, as well as IL-1β–induced secretion of MMP-1/3 by FLS and synovial SW982 cells and IL-6 by FLS, SW982 cells, human umbilical vein endothelial cells (HUVECs), and monocytic THP-1 cells, although TRYP-Ox was generally more effective and had no cytotoxicity in vitro. Evaluation of the therapeutic potential of TRYP and TRYP-Ox in vivo in murine arthritis models showed that both compounds significantly attenuated the development of collagen-induced arthritis (CIA) and collagen-antibody–induced arthritis (CAIA), with comparable efficacy. Collagen II (CII)-specific antibody levels were similarly reduced in TRYP- and TRYP-Ox-treated CIA mice. TRYP and TRYP-Ox also suppressed proinflammatory cytokine production by lymph node cells from CIA mice, with TRYP-Ox being more effective in inhibiting IL-17A, granulocyte-macrophage colony-stimulating factor (GM-CSF), and receptor activator of nuclear factor-κB ligand (RANKL). Thus, even though TRYP-Ox generally had a better in vitro profile, possibly due to its ability to inhibit c-Jun N-terminal kinase (JNK), both TRYP and TRYP-Ox were equally effective in inhibiting the clinical symptoms and damage associated with RA. Overall, TRYP and/or TRYP-Ox may represent potential new directions for the pursuit of novel treatments for RA.
has issue date	2020-07-24(xsd:dateTime)
bibo:doi	10.3389/fphar.2020.01145
has license	cc-by
sha1sum (hex)	abcbdf17d14b2d18119791c1fccedb9d671b6cfe
schema:url	https://doi.org/10.3389/fphar.2020.01145
resource representing a document's title	Therapeutic Effects of Tryptanthrin and Tryptanthrin-6-Oxime in Models of Rheumatoid Arthritis
has PubMed Central identifier	PMC7394103
schema:publication	Front Pharmacol
resource representing a document's body	covid:abcbdf17d14b2d18119791c1fccedb9d671b6cfe#body_text
is schema:about of	named entity 'HAVE' named entity 'TREATED' named entity 'IN VIVO' named entity 'ABILITY TO' named entity 'SYNTHETIC' named entity 'CYTOTOXICITY IN VITRO' named entity 'MACROPHAGES' named entity 'LYMPH NODE' named entity 'SYNOVIOCYTES' named entity 'CASES' named entity 'EFFECTIVE' named entity 'ATTENUATED' named entity 'SECRETION' named entity 'LIKE' covid:arg/abcbdf17d14b2d18119791c1fccedb9d671b6cfe named entity 'macrophages' named entity 'synoviocytes' named entity 'c-Jun N-terminal kinase' named entity 'lymph node' named entity 'JNK' named entity 'TRYP' named entity 'THP-1' named entity 'Rheumatoid Arthritis' named entity 'HUVECs' named entity 'GM-CSF' named entity 'granulocyte-macrophage colony-stimulating factor' named entity 'MMP' named entity 'mice' named entity 'FLS' named entity 'Therapeutic Effects' named entity 'Rheumatoid Arthritis' named entity 'IL-6' named entity 'CIA' named entity 'mice' named entity 'FLS' named entity 'ketone' named entity 'inflammation' named entity 'CFB' named entity 'nuclear factor' named entity 'clinical outcomes' named entity 'cartilage' named entity 'Santa Cruz, CA' named entity 'functional activity' named entity 'innate immune cells' named entity 'inflammatory disorders' named entity 'synovial cells' named entity 'pharmacological properties' named entity 'IgG' named entity 'FLS' named entity 'mice' named entity 'statistical analysis' named entity 'TRYP' named entity 'FLS' named entity 'down-regulated' named entity 'therapeutic target' named entity 'cell cultures' named entity 'therapeutic target' named entity 'arthritis' named entity 'TRYP' named entity 'mice' named entity 'macrophages' named entity 'TRYP' named entity 'CIA' named entity 'JNK' named entity 'mice' named entity 'FLS' named entity 'CIA' named entity 'IL-1b' named entity 'TRYP' named entity 'MMP1' named entity 'mice' named entity 'mice' named entity 'TRYP' named entity 'paclitaxel' named entity 'TRYP'

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