کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1977679 1061508 2008 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hepatocyte growth factor improves viability after H2O2-induced toxicity in bile duct epithelial cells
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Hepatocyte growth factor improves viability after H2O2-induced toxicity in bile duct epithelial cells
چکیده انگلیسی

Intracellular defence mechanisms against oxidative stress may play an important role in the progression of liver diseases, including cholangiopathies. The multifunctional anti-apoptotic hepatocyte growth factor (HGF) has been suggested to have antioxidant functions. The effect of HGF upon cell viability, the generation of ROS, the expression of genes that play a role in ROS defence, and the activation of caspase-3 were measured in bile duct epithelial (BDE) cells in the presence or absence of H2O2. HGF reduced H2O2-induced loss of viability, diminished H2O2-mediated ROS generation and abrogated H2O2-triggered changes in GSH/GSSG ratio. Furthermore, HGF increased the gene-expression of gamma-glutamylcysteine synthetase (GCLC) and glutathione reductase (GSR), while no effect was seen upon the gene-expression of superoxide dismutase 1 (SOD1), catalase (CAT), glutathione peroxidase (GPX1), and glutathione synthetase (GSR). Finally, HGF diminished the proteolytical activation of the key mediator of apoptosis (caspase-3) after H2O2 exposure. Together, HGF may improve viability in bile duct epithelia cells after H2O2 induced toxicity by proliferation, strengthening the intrinsic antioxidant defences, and/or by an attenuation of apoptosis. These in vitro results support the evaluation of HGF as antioxidative factor in hepatobiliary pathologies.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology - Volume 147, Issue 3, April 2008, Pages 324–330
نویسندگان
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