Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1002/jcp.26541 http://scihub22266oqcxt.onion/10.1002/jcp.26541 C6055678!6055678!29672850     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Physiol 2018 ; 233 (10): 6799-813 Nephropedia Template TP {{tp|p=29672850|t=2018. Ursolic acid ameliorates CCl4?induced liver fibrosis through the NOXs/ROS pathway |pdf=|usr=}}{{29672850}} gab.com Text Ursolic acid ameliorates CCl4 induced liver fibrosis through the NOXs/ROS pathway JO: J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29672850 #FOAvip Liver fibrosis is a reversible wound?healing response that occurs after liver injury. NADPH oxidases (NOXs) and reactive oxygen species (ROS) which are expressed in hepatocytes (HCs), hepatic stellate cells (HSCs), and Kupffer cells (KCs) play an important role in the development of hepatic fibrosis. In in vitro studies, we had shown that ursolic acid (UA) could reverse liver fibrosis by inhibiting the activation of NOX?mediated fibrotic signaling networks in HSCs. In this study, we verified that UA could alleviate CCl4?induced liver fibrosis by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Meanwhile, the phagocytic index ? and clearance index K which represent phagocytosis of KCs were unchanged. Together, all our data demonstrated that UA induced the proliferation of HCs, promoted apoptosis in HSCs, and prevented activation of KCs in vivo by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Besides, UA had no effect on the host defense function. Twit Text FOAVip Ursolic acid ameliorates CCl4 induced liver fibrosis through the NOXs/ROS pathway ????J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29672850 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29672850 #FOAvip English Wikipedia <ref>{{Cite pmid|29672850}}</ref> Ursolic acid ameliorates CCl4?induced liver fibrosis through the NOXs/ROS pathway #MMPMID29672850 Gan D; Zhang W; Huang C; Chen J; He W; Wang A; Li B; Zhu X J Cell Physiol 2018[Oct]; 233 (10): 6799-813 PMID29672850show ga Liver fibrosis is a reversible wound?healing response that occurs after liver injury. NADPH oxidases (NOXs) and reactive oxygen species (ROS) which are expressed in hepatocytes (HCs), hepatic stellate cells (HSCs), and Kupffer cells (KCs) play an important role in the development of hepatic fibrosis. In in vitro studies, we had shown that ursolic acid (UA) could reverse liver fibrosis by inhibiting the activation of NOX?mediated fibrotic signaling networks in HSCs. In this study, we verified that UA could alleviate CCl4?induced liver fibrosis by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Meanwhile, the phagocytic index ? and clearance index K which represent phagocytosis of KCs were unchanged. Together, all our data demonstrated that UA induced the proliferation of HCs, promoted apoptosis in HSCs, and prevented activation of KCs in vivo by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Besides, UA had no effect on the host defense function. äUrsolic acid ameliorates CCl4?induced liver fibrosis through the NOXs/(epmc).pdf DeepDyve Pubget Overpricing