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10.5114/aoms.2015.52371 http://scihub22266oqcxt.onion/10.5114/aoms.2015.52371 C4495160!4495160!26170860     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26170860&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arch+Med+Sci 2015 ; 11 (3): 647-53 Nephropedia Template TP {{tp|p=26170860|t=2015. Blockade of CCN4 attenuates CCl4-induced liver fibrosis |pdf=|usr=}}{{26170860}} gab.com Text Blockade of CCN4 attenuates CCl4-induced liver fibrosis JO: Arch Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=26170860 #FOAvip Introduction: CCN4, also termed WNT-inducible signaling pathway protein-1 (WISP-1), has important roles in inflammation and tissue injury. This study aimed to investigate the effect of CCN4 inhibition using monoclonal anti-CCN4 antibody (CCN4mAb) on the liver injury and fibrosis in a mouse model of liver fibrosis. Material and methods: The mouse liver fibrosis model was induced by carbon tetrachloride (CCl4). Mice received vehicle (saline/olive oil) by subcutaneous injection, CCl4 by subcutaneous injection or CCl4 (subcutaneous) plus CCN4mAb by subcutaneous injection. The pro-inflammatory and pro-fibrotic factors were determined by Western blot. The biochemistry and histopathology, collagen deposition and nuclear factor (NF)-?B activity were also assessed. Results: Chronic CCl4 treatment caused liver injury and collagen accumulation. The expression levels of CCN4, pro-inflammatory and pro-fibrotic mediators as well as the activity of NF-?B were markedly increased. Treatment with CCN4mAb significantly inhibited CCl4-induced CCN4 expression, leading to attenuated CCl4-induced liver injury and the inflammatory response. CCN4 blockade also significantly reduced the formation of collagen in the liver and the expression of ?-smooth muscle actin and transforming growth factor ?1. Conclusions: CCN4 inhibition by CCN4mAb in vivo significantly attenuated the CCl4-induced liver injury and the progression of liver fibrosis. CCN4 may represent a novel therapeutic target for liver injury and fibrosis. Twit Text FOAVip Blockade of CCN4 attenuates CCl4-induced liver fibrosis ????Arch Med Sci http://www.kidney.de/pget.php?&tw=1&pmid=26170860 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26170860 #FOAvip English Wikipedia <ref>{{Cite pmid|26170860}}</ref> Blockade of CCN4 attenuates CCl4-induced liver fibrosis #MMPMID26170860 Li X; Chen Y; Ye W; Tao X; Zhu J; Wu S; Lou L Arch Med Sci 2015[Jun]; 11 (3): 647-53 PMID26170860show ga Introduction: CCN4, also termed WNT-inducible signaling pathway protein-1 (WISP-1), has important roles in inflammation and tissue injury. This study aimed to investigate the effect of CCN4 inhibition using monoclonal anti-CCN4 antibody (CCN4mAb) on the liver injury and fibrosis in a mouse model of liver fibrosis. Material and methods: The mouse liver fibrosis model was induced by carbon tetrachloride (CCl4). Mice received vehicle (saline/olive oil) by subcutaneous injection, CCl4 by subcutaneous injection or CCl4 (subcutaneous) plus CCN4mAb by subcutaneous injection. The pro-inflammatory and pro-fibrotic factors were determined by Western blot. The biochemistry and histopathology, collagen deposition and nuclear factor (NF)-?B activity were also assessed. Results: Chronic CCl4 treatment caused liver injury and collagen accumulation. The expression levels of CCN4, pro-inflammatory and pro-fibrotic mediators as well as the activity of NF-?B were markedly increased. Treatment with CCN4mAb significantly inhibited CCl4-induced CCN4 expression, leading to attenuated CCl4-induced liver injury and the inflammatory response. CCN4 blockade also significantly reduced the formation of collagen in the liver and the expression of ?-smooth muscle actin and transforming growth factor ?1. Conclusions: CCN4 inhibition by CCN4mAb in vivo significantly attenuated the CCl4-induced liver injury and the progression of liver fibrosis. CCN4 may represent a novel therapeutic target for liver injury and fibrosis. äBlockade of CCN4 attenuates CCl4-induced liver fibrosis (epmc).pdf DeepDyve Pubget Overpricing