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10.14814/phy2.12757 http://scihub22266oqcxt.onion/10.14814/phy2.12757 C4831326!4831326 !27081162     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27081162 &cmd=llinks): Failed to open stream: HTTP request failed! 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N-acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure |pdf=|usr=}}{{27081162 }} gab.com Text N-acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27081162 #FOAvip Oxidative stress plays a central role in the pathogenesis of heart failure. We aimed to determine whether the antioxidantN-acetylcysteine can attenuate cardiac fibrosis and remodeling in a mouse model of heart failure. Minipumps were implanted subcutaneously in wild-type mice (n = 20) and mice with cardiomyopathy secondary to cardiac specific overexpression of mammalian sterile 20-like kinase 1 (MST-1;n = 18) to administerN-acetylcysteine (40 mg/kg per day) or saline for a period of 8 weeks. At the end of this period, cardiac remodeling and function was assessed via echocardiography. Fibrosis, oxidative stress, and expression of collagen types I andIIIwere quantified in heart tissues. Cardiac perivascular and interstitial fibrosis were greater by 114% and 209%, respectively, inMST-1 compared to wild type (P ? 0.001). InMST-1 mice administeredN-acetylcysteine, perivascular and interstitial fibrosis were 40% and 57% less, respectively, compared to those treated with saline (P ? 0. 03). Cardiac oxidative stress was 119% greater inMST-1 than in wild type (P < 0.001) andN-acetylcysteine attenuated oxidative stress inMST-1 by 42% (P = 0.005). These data indicate thatN-acetylcysteine can blunt cardiac fibrosis and related remodeling in the setting of heart failure potentially by reducing oxidative stress. This study provides the basis to investigate the role ofN-acetylcysteine in chronic heart failure. Twit Text FOAVip N-acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27081162 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27081162 #FOAvip English Wikipedia <ref>{{Cite pmid|27081162 }}</ref> N-acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure #MMPMID27081162 Giam B ; Chu PY ; Kuruppu S ; Smith AI ; Horlock D ; Kiriazis H ; Du XJ ; Kaye DM ; Rajapakse NW Physiol Rep 2016[Apr]; 4 (7 ): ä PMID27081162 show ga Oxidative stress plays a central role in the pathogenesis of heart failure. We aimed to determine whether the antioxidantN-acetylcysteine can attenuate cardiac fibrosis and remodeling in a mouse model of heart failure. Minipumps were implanted subcutaneously in wild-type mice (n = 20) and mice with cardiomyopathy secondary to cardiac specific overexpression of mammalian sterile 20-like kinase 1 (MST-1;n = 18) to administerN-acetylcysteine (40 mg/kg per day) or saline for a period of 8 weeks. At the end of this period, cardiac remodeling and function was assessed via echocardiography. Fibrosis, oxidative stress, and expression of collagen types I andIIIwere quantified in heart tissues. Cardiac perivascular and interstitial fibrosis were greater by 114% and 209%, respectively, inMST-1 compared to wild type (P ? 0.001). InMST-1 mice administeredN-acetylcysteine, perivascular and interstitial fibrosis were 40% and 57% less, respectively, compared to those treated with saline (P ? 0. 03). Cardiac oxidative stress was 119% greater inMST-1 than in wild type (P < 0.001) andN-acetylcysteine attenuated oxidative stress inMST-1 by 42% (P = 0.005). These data indicate thatN-acetylcysteine can blunt cardiac fibrosis and related remodeling in the setting of heart failure potentially by reducing oxidative stress. This study provides the basis to investigate the role ofN-acetylcysteine in chronic heart failure. |Acetylcysteine/*pharmacology [MESH] |Animals [MESH] |Antioxidants/*pharmacology [MESH] |Collagen Type I/metabolism [MESH] |Collagen Type III/metabolism [MESH] |Disease Models, Animal [MESH] |Fibrosis [MESH] |Genetic Predisposition to Disease [MESH] |Heart Failure/diagnostic imaging/*drug therapy/enzymology/genetics/physiopathology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Myocytes, Cardiac/*drug effects/metabolism/pathology [MESH] |Oxidative Stress/*drug effects [MESH] |Phenotype [MESH] |Protein Serine-Threonine Kinases/genetics/metabolism [MESH] |Time Factors [MESH] |Ultrasonography [MESH] |Ventricular Function, Left/*drug effects [MESH]N-acetylcysteine attenuates the development of cardiac fibrosis and re(epmc).pdf DeepDyve Pubget Overpricing