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10.1016/j.phrs.2020.105223 http://scihub22266oqcxt.onion/10.1016/j.phrs.2020.105223 33017650!7530556!33017650     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Pharmacol+Res 2020 ; 161 (ä): 105223 Nephropedia Template TP {{tp|p=33017650|t=2020. Activation of angiotensin II type-2 receptor protects against cigarette smoke-induced COPD |pdf=|usr=}}{{33017650}} gab.com Text Activation of angiotensin II type-2 receptor protects against cigarette smoke-induced COPD JO: Pharmacol Res http://www.kidney.de/pget.php?&tw=1&pmid=33017650 #FOAvip Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally. Cumulative evidence has implicated renin-angiotensin system (RAS) in the pathogenesis of COPD. This study aimed to investigate potential protective effects of angiotensin II type-2 receptor (AT2R) activation in cigarette smoke (CS)-induced COPD models. Compound 21 (C21), a selective and potent non-peptide small molecule AT2R agonist, was evaluated for anti-inflammatory, anti-oxidative and anti-remodeling activities in a two-week (acute) and an eight-week (chronic) CS-induced COPD models. C21 inhibited CS-induced increases in macrophage and neutrophil counts, pro-inflammatory cytokines and oxidative damage markers in bronchoalveolar lavage (BAL) fluid, and TGF-beta1 in lung tissues, from COPD models. C21 restored phosphatase activities and reduced phospho-p38 MAPK, phospho-ERK and p65 subunit of NF-kappaB levels in CS-exposed lung tissues. C21 also suppressed CS-induced increases in alpha-Sma, Mmp9, Mmp12 and hydroxyproline levels in lung tissues, and neutrophil elastase activity in BAL fluid. C21 modulated RAS in CS-exposed lungs by downregulating Ang II but upregulating Ang-(1-7) and Mas receptor levels. C21 prevented CS-induced emphysema and improved lung functions in chronic COPD model. We report here for the first time the protective effects of AT2R agonist C21 against CS-induced COPD, and provide strong evidence for further development of AT2R agonist for the treatment of COPD. Twit Text FOAVip Activation of angiotensin II type-2 receptor protects against cigarette smoke-induced COPD ????Pharmacol Res http://www.kidney.de/pget.php?&tw=1&pmid=33017650 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33017650 #FOAvip English Wikipedia <ref>{{Cite pmid|33017650}}</ref> Activation of angiotensin II type-2 receptor protects against cigarette smoke-induced COPD #MMPMID33017650 Mei D; Tan WSD; Liao W; Heng CKM; Wong WSF Pharmacol Res 2020[Nov]; 161 (ä): 105223 PMID33017650show ga Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally. Cumulative evidence has implicated renin-angiotensin system (RAS) in the pathogenesis of COPD. This study aimed to investigate potential protective effects of angiotensin II type-2 receptor (AT2R) activation in cigarette smoke (CS)-induced COPD models. Compound 21 (C21), a selective and potent non-peptide small molecule AT2R agonist, was evaluated for anti-inflammatory, anti-oxidative and anti-remodeling activities in a two-week (acute) and an eight-week (chronic) CS-induced COPD models. C21 inhibited CS-induced increases in macrophage and neutrophil counts, pro-inflammatory cytokines and oxidative damage markers in bronchoalveolar lavage (BAL) fluid, and TGF-beta1 in lung tissues, from COPD models. C21 restored phosphatase activities and reduced phospho-p38 MAPK, phospho-ERK and p65 subunit of NF-kappaB levels in CS-exposed lung tissues. C21 also suppressed CS-induced increases in alpha-Sma, Mmp9, Mmp12 and hydroxyproline levels in lung tissues, and neutrophil elastase activity in BAL fluid. C21 modulated RAS in CS-exposed lungs by downregulating Ang II but upregulating Ang-(1-7) and Mas receptor levels. C21 prevented CS-induced emphysema and improved lung functions in chronic COPD model. We report here for the first time the protective effects of AT2R agonist C21 against CS-induced COPD, and provide strong evidence for further development of AT2R agonist for the treatment of COPD. |Airway Remodeling/drug effects[MESH] |Angiotensin I/metabolism[MESH] |Angiotensin II/metabolism[MESH] |Animals[MESH] |Anti-Inflammatory Agents/*pharmacology[MESH] |Antioxidants/*pharmacology[MESH] |Cytokines/metabolism[MESH] |Disease Models, Animal[MESH] |Female[MESH] |Imidazoles/*pharmacology[MESH] |Inflammation Mediators/metabolism[MESH] |Lung/*drug effects/metabolism/physiopathology[MESH] |Macrophages, Alveolar/drug effects/metabolism[MESH] |Mice, Inbred BALB C[MESH] |Neutrophils/drug effects/metabolism[MESH] |Oxidative Stress/drug effects[MESH] |Peptide Fragments/metabolism[MESH] |Proto-Oncogene Mas[MESH] |Proto-Oncogene Proteins[MESH] |Pulmonary Disease, Chronic Obstructive/etiology/metabolism/physiopathology/*prevention & control[MESH] |Pulmonary Emphysema/etiology/metabolism/physiopathology/*prevention & control[MESH] |Receptor, Angiotensin, Type 2/*agonists/metabolism[MESH] |Receptors, G-Protein-Coupled[MESH] |Renin-Angiotensin System/*drug effects[MESH] |Signal Transduction[MESH] |Smoke[MESH] |Sulfonamides/*pharmacology[MESH] |Thiophenes/*pharmacology[MESH]Activation of angiotensin II type-2 receptor protects against cigarett(epmc).pdf DeepDyve Pubget Overpricing