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10.1038/srep26928 http://scihub22266oqcxt.onion/10.1038/srep26928 C4882609!4882609 !27229886     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27229886 &cmd=llinks): Failed to open stream: HTTP request failed! 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The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease |pdf=|usr=}}{{27229886 }} gab.com Text The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27229886 #FOAvip COPD is characterized by persistent airflow limitation, neutrophilia and oxidative stress from endogenous and exogenous insults. Current COPD therapy involving anticholinergics, ?2-adrenoceptor agonists and/or corticosteroids, do not specifically target oxidative stress, nor do they reduce chronic pulmonary inflammation and disease progression in all patients. Here, we explore the effects of Sul-121, a novel compound with anti-oxidative capacity, on hyperresponsiveness (AHR) and inflammation in experimental models of COPD. Using a guinea pig model of lipopolysaccharide (LPS)-induced neutrophilia, we demonstrated that Sul-121 inhalation dose-dependently prevented LPS-induced airway neutrophilia (up to ~60%) and AHR (up to ~90%). Non-cartilaginous airways neutrophilia was inversely correlated with blood H2S, and LPS-induced attenuation of blood H2S (~60%) was prevented by Sul-121. Concomitantly, Sul-121 prevented LPS-induced production of the oxidative stress marker, malondialdehyde by ~80%. In immortalized human airway smooth muscle (ASM) cells, Sul-121 dose-dependently prevented cigarette smoke extract-induced IL-8 release parallel with inhibition of nuclear translocation of the NF-?B subunit, p65 (each ~90%). Sul-121 also diminished cellular reactive oxygen species production in ASM cells, and inhibited nuclear translocation of the anti-oxidative response regulator, Nrf2. Our data show that Sul-121 effectively inhibits airway inflammation and AHR in experimental COPD models, prospectively through inhibition of oxidative stress. Twit Text FOAVip The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27229886 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27229886 #FOAvip English Wikipedia <ref>{{Cite pmid|27229886 }}</ref> The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease #MMPMID27229886 Han B ; Poppinga WJ ; Zuo H ; Zuidhof AB ; Bos IS ; Smit M ; Vogelaar P ; Krenning G ; Henning RH ; Maarsingh H ; Halayko AJ ; van Vliet B ; Stienstra S ; Graaf AC ; Meurs H ; Schmidt M Sci Rep 2016[May]; 6 (ä): 26928 PMID27229886 show ga COPD is characterized by persistent airflow limitation, neutrophilia and oxidative stress from endogenous and exogenous insults. Current COPD therapy involving anticholinergics, ?2-adrenoceptor agonists and/or corticosteroids, do not specifically target oxidative stress, nor do they reduce chronic pulmonary inflammation and disease progression in all patients. Here, we explore the effects of Sul-121, a novel compound with anti-oxidative capacity, on hyperresponsiveness (AHR) and inflammation in experimental models of COPD. Using a guinea pig model of lipopolysaccharide (LPS)-induced neutrophilia, we demonstrated that Sul-121 inhalation dose-dependently prevented LPS-induced airway neutrophilia (up to ~60%) and AHR (up to ~90%). Non-cartilaginous airways neutrophilia was inversely correlated with blood H2S, and LPS-induced attenuation of blood H2S (~60%) was prevented by Sul-121. Concomitantly, Sul-121 prevented LPS-induced production of the oxidative stress marker, malondialdehyde by ~80%. In immortalized human airway smooth muscle (ASM) cells, Sul-121 dose-dependently prevented cigarette smoke extract-induced IL-8 release parallel with inhibition of nuclear translocation of the NF-?B subunit, p65 (each ~90%). Sul-121 also diminished cellular reactive oxygen species production in ASM cells, and inhibited nuclear translocation of the anti-oxidative response regulator, Nrf2. Our data show that Sul-121 effectively inhibits airway inflammation and AHR in experimental COPD models, prospectively through inhibition of oxidative stress. |Animals [MESH] |Anti-Inflammatory Agents, Non-Steroidal/*pharmacology [MESH] |Antioxidants/*pharmacology [MESH] |Cell Line, Transformed [MESH] |Chromans/chemistry/*pharmacology [MESH] |Complex Mixtures/antagonists & inhibitors/pharmacology [MESH] |Disease Models, Animal [MESH] |Gene Expression Regulation [MESH] |Guinea Pigs [MESH] |Humans [MESH] |Hydrogen Sulfide/agonists/blood [MESH] |Hypersensitivity/etiology/immunology/metabolism/*prevention & control [MESH] |Inflammation [MESH] |Interleukin-8/antagonists & inhibitors/genetics/immunology [MESH] |Lipopolysaccharides/administration & dosage [MESH] |Lung [MESH] |Male [MESH] |Malondialdehyde/antagonists & inhibitors/metabolism [MESH] |Myocytes, Smooth Muscle/drug effects/immunology/pathology [MESH] |NF-E2-Related Factor 2/antagonists & inhibitors/genetics/immunology [MESH] |Neutrophils/drug effects/immunology/pathology [MESH] |Oxidative Stress [MESH] |Piperazines/chemistry/*pharmacology [MESH] |Pulmonary Disease, Chronic Obstructive/*drug therapy/immunology/metabolism/physiopathology [MESH] |Reactive Oxygen Species/*antagonists & inhibitors/metabolism [MESH] |Tars/chemistry/toxicity [MESH]The novel compound Sul-121 inhibits airway inflammation and hyperrespo(epmc).pdf DeepDyve Pubget Overpricing