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RISS 인기검색어
- 검색키워드
- 저자 : Iwaisako, Keiko (검색결과 2 건)
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LC, Acute : O-055 ; Protection from liver fibrosis by a PPAR agonist
( Keiko Iwaisako ),( Yong Han Paik ),( Michael Haimer ),( Kojiro Taura ),( Yuzo Kodama ),( Claude Sirlin ),( Elizabeth Yu ),( Ruth T Yu ),( Michael Downes ),( Ronald M Evans ),( David A Brenner ),( Be 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.1
Background: Peroxisome Proliferator-Activated Receptor delta (PPAR), a member of the nuclear receptor family, is emerging as a key metabolic regulator with pleiotropic actions on various tissues including fat, skeletal muscle and liver. The aim of our study was to assess the effect of a new and highly selective PPAR agonist KD3010 in experimental mouse models of liver fibrosis induced by carbon tetrachloride (CCl4) injections or bile duct ligation (BDL). Methods: Male adult C57/B6 mice were treated daily with vehicle or KD3010 by oral gavage. Liver fibrosis was induced by repeated intraperitoneal injections of CCl4 or BDL. For in vitro study, primary hepatocytes were isolated and incubated with/without KD3010. Results: PPAR agonist KD3010 ameliorates liver injury induced by CCl4 injections. Deposition of extracellular matrix proteins was lower in the KD3010 group as compared to the control group. The hepatoprotective and antifibrotic effect of KD3010 was confirmed in a model of cholestasis-induced liver injury and fibrosis using BDL for three weeks. Primary hepatocytes incubated with KD3010 were protected from serum starvation or CCl4-induced cell death, in part due to reduced reactive oxygen species (ROS) production. Conclusions: The PPAR agonist KD3010 has hepatoprotective and antifibrotic effects in animal models of liver fibrosis suggesting a new mechanistic and therapeutic approach in treating patients with chronic liver diseases.
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Paik, Yong‐,Han,Iwaisako, Keiko,Seki, Ekihiro,Inokuchi, Sayaka,Schnabl, Bernd,Ö,sterreicher, Christoph H.,Kisseleva, Tatiana,Brenner, David A. Wiley Subscription Services, Inc., A Wiley Company 2011 Hepatology Vol.53 No.5
<P><B>Abstract</B></P><P>Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multicomponent enzyme that mediates electron transfer from nicotinamide adenine dinucleotide phosphate to molecular oxygen, which leads to the production of superoxide. NOX2/gp91<SUP>phox</SUP> is a catalytic subunit of NOX expressed in phagocytic cells. Several homologues of NOX2, including NOX1, have been identified in nonphagocytic cells. We investigated the contributory role of NOX1 and NOX2 in hepatic fibrosis. Hepatic fibrosis was induced in wild‐type (WT) mice, NOX1 knockout (NOX1KO) mice, and NOX2 knockout (NOX2KO) mice by way of either carbon tetrachloride (CCl<SUB>4</SUB>) injection or bile duct ligation (BDL). The functional contribution of NOX1 and NOX2 in endogenous liver cells, including hepatic stellate cells (HSCs), and bone marrow (BM)‐derived cells, including Kupffer cells (KCs), to hepatic reactive oxygen species (ROS) generation and hepatic fibrosis was assessed <I>in vitro</I> and <I>in vivo</I> using NOX1 or NOX2 BM chimeric mice. Hepatic NOX1 and NOX2 messenger RNA expression was increased in the two experimental mouse models of hepatic fibrosis. Whereas NOX1 was expressed in HSCs but not in KCs, NOX2 was expressed in both HSCs and KCs. Hepatic fibrosis and ROS generation were attenuated in both NOX1KO and NOX2KO mice after CCl<SUB>4</SUB> or BDL. Liver fibrosis in chimeric mice indicated that NOX1 mediates the profibrogenic effects in endogenous liver cells, whereas NOX2 mediates the profibrogenic effects in both endogenous liver cells and BM‐derived cells. Multiple NOX1 and NOX2 components were up‐regulated in activated HSCs. Both NOX1‐ and NOX2‐deficient HSCs had decreased ROS generation and failed to up‐regulate collagen α1(I) and transforming growth factor β in response to angiotensin II. <I>Conclusion:</I> Both NOX1 and NOX2 have an important role in hepatic fibrosis in endogenous liver cells, including HSCs, whereas NOX2 has a lesser role in BM‐derived cells. (H<SMALL>EPATOLOGY</SMALL> 2011;)</P>
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