کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8258785 | 1534613 | 2018 | 35 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibition of EGFR attenuates fibrosis and stellate cell activation in diet-induced model of nonalcoholic fatty liver disease
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کلمات کلیدی
DCFH-DAAdipoSREBPACCALTBTCCTGFALBDcf2′,7′-dichlorofluorescein - 2 '، 7'-dichlorofluoresceinADAM - آدامadiponectin - آدیپونکتینAST - آسپارتات ترانس آمینازalanine transaminase - آلانین ترانس آمینازAlbumin - آلبومینALP - آلکالن فسفاتازAlkaline phosphatase - آلکالین فسفاتاز یا فسفاتاز قلیاییacetyl coA carboxylase - استیل کولا کربوکسیلازa disintegrin and metalloproteinases - تخریب و متالوپروتئینازaspartate transaminase - ترانس آمیناز آسپارتاتConnective tissue growth factor - فاکتور رشد بافت همبندSterol regulatory element-binding protein - پروتئین اتصال دهنده پروتئین Sterol RegulatoryCollagen - کلاژنcol - کول
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. NAFLD begins with steatosis and advances to nonalcoholic steatohepatitis (NASH) and cirrhosis. The molecular mechanisms involved in NAFLD progression are not understood. Based on recent studies showing dysregulation of epidermal growth factor receptor (EGFR) in animal models of liver injury, we sought to determine if inhibition of EGFR mitigates liver fibrosis and HSC activation in NAFLD. We utilized the high fat diet (HFD)-induced murine model of liver injury to study the role of EGFR in NAFLD. The lipid accumulation, oxidative stress, hepatic stellate cell (HSC) activation and matrix deposition were examined in the liver tissues. We also evaluated the EGFR signaling pathway, ROS activation and pro-fibrogenic phenotype in oxidized low density lipoproteins (ox-LDL) challenged cultured HSCs. We demonstrate that EGFR was phosphorylated in liver tissues of HFD murine model of NAFLD. Inhibition of EGFR prevented diet-induced lipid accumulation, oxidative stress, and HSC activation and matrix deposition. In cultured HSCs, we show that ox-LDL caused rapid activation of the EGFR signaling pathway and induce the production of reactive oxygen species. EGFR also mediated HSC activation and promoted a pro-fibrogenic phenotype. In conclusion, our data demonstrate that EGFR plays an important role in NAFLD and is an attractive target for NAFLD therapy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 1, January 2018, Pages 133-142
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 1, January 2018, Pages 133-142
نویسندگان
Dandan Liang, Hongjin Chen, Leping Zhao, Wenxin Zhang, Jie Hu, Zhiguo Liu, Peng Zhong, Wei Wang, Jingying Wang, Guang Liang,