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10.1111/jcmm.12898 http://scihub22266oqcxt.onion/10.1111/jcmm.12898 C5082399!5082399 !27306439     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27306439 &cmd=llinks): Failed to open stream: HTTP request failed! 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Fluorofenidone attenuates pulmonary inflammation and fibrosis via inhibiting the activation of NALP3 inflammasome and IL-1?/IL-1R1/MyD88/NF-?B pathway |pdf=|usr=}}{{27306439 }} gab.com Text Fluorofenidone attenuates pulmonary inflammation and fibrosis via inhibiting the activation of NALP3 inflammasome and IL-1 /IL-1R1/MyD88/NF- B pathway JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27306439 #FOAvip Interleukin (IL)-1? plays an important role in the pathogenesis of idiopathic pulmonary fibrosis. The production of IL-1? is dependent upon caspase-1-containing multiprotein complexes called inflammasomes and IL-1R1/MyD88/NF-?B pathway. In this study, we explored whether a potential anti-fibrotic agent fluorofenidone (FD) exerts its anti-inflammatory and anti-fibrotic effects through suppressing activation of NACHT, LRR and PYD domains-containing protein 3 (NALP3) inflammasome and the IL-1?/IL-1R1/MyD88/NF-?B pathway in vivo and in vitro. Male C57BL/6J mice were intratracheally injected with Bleomycin (BLM) or saline. Fluorofenidone was administered throughout the course of the experiment. Lung tissue sections were stained with haemotoxylin and eosin and Masson's trichrome. Cytokines were measured by ELISA, and ?-smooth muscle actin (?-SMA), fibronectin, collagen I, caspase-1, IL-1R1, MyD88 were measured by Western blot and/or RT-PCR. The human actue monocytic leukaemia cell line (THP-1) were incubated with monosodium urate (MSU), with or without FD pre-treatment. The expression of caspase-1, IL-1?, NALP3, apoptosis-associated speck-like protein containing (ASC) and pro-caspase-1 were measured by Western blot, the reactive oxygen species (ROS) generation was detected using the Flow Cytometry, and the interaction of NALP3 inflammasome-associated molecules were measured by Co-immunoprecipitation. RLE-6TN (rat lung epithelial-T-antigen negative) cells were incubated with IL-1?, with or without FD pre-treatment. The expression of nuclear protein p65 was measured by Western blot. Results showed that FD markedly reduced the expressions of IL-1?, IL-6, monocyte chemotactic protein-1 (MCP-1), myeloperoxidase (MPO), ?-SMA, fibronectin, collagen I, caspase-1, IL-1R1 and MyD88 in mice lung tissues. And FD inhibited MSU-induced the accumulation of ROS, blocked the interaction of NALP3 inflammasome-associated molecules, decreased the level of caspase-1 and IL-1? in THP-1 cells. Besides, FD inhibited IL-1?-induced the expression of nuclear protein p65. This study demonstrated that FD, attenuates BLM-induced pulmonary inflammation and fibrosis in mice via inhibiting the activation of NALP3 inflammasome and the IL-1?/IL-1R1/MyD88/ NF-?B pathway. Twit Text FOAVip Fluorofenidone attenuates pulmonary inflammation and fibrosis via inhibiting the activation of NALP3 inflammasome and IL-1 /IL-1R1/MyD88/NF- B pathway ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27306439 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27306439 #FOAvip English Wikipedia <ref>{{Cite pmid|27306439 }}</ref> Fluorofenidone attenuates pulmonary inflammation and fibrosis via inhibiting the activation of NALP3 inflammasome and IL-1?/IL-1R1/MyD88/NF-?B pathway #MMPMID27306439 Song C ; He L ; Zhang J ; Ma H ; Yuan X ; Hu G ; Tao L ; Zhang J ; Meng J J Cell Mol Med 2016[Nov]; 20 (11 ): 2064-2077 PMID27306439 show ga Interleukin (IL)-1? plays an important role in the pathogenesis of idiopathic pulmonary fibrosis. The production of IL-1? is dependent upon caspase-1-containing multiprotein complexes called inflammasomes and IL-1R1/MyD88/NF-?B pathway. In this study, we explored whether a potential anti-fibrotic agent fluorofenidone (FD) exerts its anti-inflammatory and anti-fibrotic effects through suppressing activation of NACHT, LRR and PYD domains-containing protein 3 (NALP3) inflammasome and the IL-1?/IL-1R1/MyD88/NF-?B pathway in vivo and in vitro. Male C57BL/6J mice were intratracheally injected with Bleomycin (BLM) or saline. Fluorofenidone was administered throughout the course of the experiment. Lung tissue sections were stained with haemotoxylin and eosin and Masson's trichrome. Cytokines were measured by ELISA, and ?-smooth muscle actin (?-SMA), fibronectin, collagen I, caspase-1, IL-1R1, MyD88 were measured by Western blot and/or RT-PCR. The human actue monocytic leukaemia cell line (THP-1) were incubated with monosodium urate (MSU), with or without FD pre-treatment. The expression of caspase-1, IL-1?, NALP3, apoptosis-associated speck-like protein containing (ASC) and pro-caspase-1 were measured by Western blot, the reactive oxygen species (ROS) generation was detected using the Flow Cytometry, and the interaction of NALP3 inflammasome-associated molecules were measured by Co-immunoprecipitation. RLE-6TN (rat lung epithelial-T-antigen negative) cells were incubated with IL-1?, with or without FD pre-treatment. The expression of nuclear protein p65 was measured by Western blot. Results showed that FD markedly reduced the expressions of IL-1?, IL-6, monocyte chemotactic protein-1 (MCP-1), myeloperoxidase (MPO), ?-SMA, fibronectin, collagen I, caspase-1, IL-1R1 and MyD88 in mice lung tissues. And FD inhibited MSU-induced the accumulation of ROS, blocked the interaction of NALP3 inflammasome-associated molecules, decreased the level of caspase-1 and IL-1? in THP-1 cells. Besides, FD inhibited IL-1?-induced the expression of nuclear protein p65. This study demonstrated that FD, attenuates BLM-induced pulmonary inflammation and fibrosis in mice via inhibiting the activation of NALP3 inflammasome and the IL-1?/IL-1R1/MyD88/ NF-?B pathway. |*Signal Transduction/drug effects [MESH] |Actins/metabolism [MESH] |Animals [MESH] |Bleomycin [MESH] |Caspase 1/metabolism [MESH] |Chemokine CCL2/metabolism [MESH] |Collagen Type I/metabolism [MESH] |Down-Regulation/drug effects [MESH] |Fibronectins/metabolism [MESH] |Humans [MESH] |Inflammasomes/*metabolism [MESH] |Interleukin-1beta/metabolism [MESH] |Interleukin-6/metabolism [MESH] |Lung/drug effects/metabolism/pathology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Myeloid Differentiation Factor 88 [MESH] |NF-kappa B/metabolism [MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/*metabolism [MESH] |Peroxidase/metabolism [MESH] |Pneumonia/chemically induced/*complications/*drug therapy/metabolism [MESH] |Pulmonary Fibrosis/*complications/*drug therapy/metabolism/pathology [MESH] |Pyridones/pharmacology/*therapeutic use [MESH] |Reactive Oxygen Species/metabolism [MESH] |Receptors, Interleukin/metabolism [MESH]Fluorofenidone attenuates pulmonary inflammation and fibrosis via inhi(epmc).pdf DeepDyve Pubget Overpricing