Toxicoproteomic analysis of phalloidin-induced cholestasis in mouse liver
| Autor: | Myung-Sang Kwon, Seokjoo Yoon, Sun Hee Heo, Suresh V. S. Rana, Han-Jin Park, Jung-Hwa Oh |
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| Rok vydání: | 2010 |
| Předmět: |
medicine.diagnostic_test
biology Phalloidin Health Toxicology and Mutagenesis Public Health Environmental and Occupational Health Lipid metabolism macromolecular substances Toxicology Microfilament medicine.disease Hsp90 Molecular biology Pathology and Forensic Medicine chemistry.chemical_compound Western blot Cholestasis chemistry Gluconeogenesis medicine biology.protein sense organs General Pharmacology Toxicology and Pharmaceutics Cytoskeleton |
| Zdroj: | Molecular & Cellular Toxicology. 6:87-95 |
| ISSN: | 2092-8467 1738-642X |
| DOI: | 10.1007/s13273-010-0012-7 |
| Popis: | Phalloidin induces cholestasis by preventing microfilament depolymerization. Phalloidin has been widely used as an agent to induce intrahepatic cholestasis in experimental animals. The objective of this study was to examine the effects of phalloidin on protein expression profiles in mouse liver, so as to identify potential biomarkers of intrahepatic cholestasis. Phalloidin was administered to BALB/c mice at a predetermined dose of 1 mg/kg for 7 days, and phalloidin-induced cholestasis was observed. Hepatic protein expression was investigated via two-dimensional (2D) electrophoresis, and 21 protein spots showing significantly different expression between the treated and control groups were excised from the gels and identified by MALDI-TOF/TOF. The identified proteins were involved in cytoskeletal changes, lipid metabolism, gluconeogenesis, detoxification, and transport mechanisms. Among these proteins, the up-regulation of HSP90-β in phalloidin-treated mice was confirmed by Western blot analysis and then by RT-PCR, indicating that it may serve as a useful biomarker of cholestasis. In summary, these results provide insight into the mechanism involved in phalloidin-induced cytoskeletal change and cholestasis. |
| Databáze: | OpenAIRE |
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