Induction of heme oxygenase-1 protects mouse liver from apoptotic ischemia/reperfusion injury
العنوان: | Induction of heme oxygenase-1 protects mouse liver from apoptotic ischemia/reperfusion injury |
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المؤلفون: | G. Abraham Nader, O. Pappo, Michal Safran, Ran Kornowski, Y. Katz, Yossi Issan, Franklin Grief, Laniado-Schwartzman Michal, Ziv Ben-Ari, Maya Sultan, Edith Hochhauser |
المصدر: | Apoptosis. 18:547-555 |
بيانات النشر: | Springer Science and Business Media LLC, 2013. |
سنة النشر: | 2013 |
مصطلحات موضوعية: | Male, Cancer Research, Pathology, medicine.medical_specialty, medicine.medical_treatment, Clinical Biochemistry, Ischemia, Gene Expression, Protoporphyrins, Pharmaceutical Science, Primary Graft Dysfunction, Apoptosis, Liver transplantation, Pharmacology, Article, Inhibitor of Apoptosis Proteins, Mice, medicine, Animals, Caspase 3, business.industry, Biochemistry (medical), Membrane Proteins, Cell Biology, medicine.disease, COPP, Cytoprotection, Heme oxygenase, Ki-67 Antigen, Liver, Enzyme Induction, Reperfusion Injury, CCAAT-Enhancer-Binding Proteins, Hepatocytes, business, Reperfusion injury, Biomarkers, Heme Oxygenase-1, Injections, Intraperitoneal |
الوصف: | Ischemia/reperfusion (I/R) injury is the main cause of primary graft dysfunction of liver allografts. Cobalt-protoporphyrin (CoPP)–dependent induction of heme oxygenase (HO)-1 has been shown to protect the liver from I/R injury. This study analyzes the apoptotic mechanisms of HO-1-mediated cytoprotection in mouse liver exposed to I/R injury. HO-1 induction was achieved by the administration of CoPP (1.5 mg/kg body weight i.p.). Mice were studied in in vivo model of hepatic segmental (70 %) ischemia for 60 min and reperfusion injury. Mice were randomly allocated to four main experimental groups (n = 10 each): (1) A control group undergoing sham operation. (2) Similar to group 1 but with the administration of CoPP 72 h before the operation. (3) Mice undergoing in vivo hepatic I/R. (4) Similar to group 3 but with the administration of CoPP 72 h before ischemia induction. When compared with the I/R mice group, in the I/R+CoPP mice group, the increased hepatic expression of HO-1 was associated with a significant reduction in liver enzyme levels, fewer apoptotic hepatocytes cells were identified by morphological criteria and by immunohistochemistry for caspase-3, there was a decreased mean number of proliferating cells (positively stained for Ki67), and a reduced hepatic expression of: C/EBP homologous protein (an index of endoplasmic reticulum stress), the NF-κB’s regulated genes (CIAP2, MCP-1 and IL-6), and increased hepatic expression of IκBa (the inhibitory protein of NF-κB). HO-1 over-expression plays a pivotal role in reducing the hepatic apoptotic IR injury. HO-1 may serve as a potential target for therapeutic intervention in hepatic I/R injury during liver transplantation. |
تدمد: | 1573-675X 1360-8185 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d9fdebbe5f1b52238f364b12ab693120 https://doi.org/10.1007/s10495-013-0814-x |
حقوق: | OPEN |
رقم الأكسشن: | edsair.doi.dedup.....d9fdebbe5f1b52238f364b12ab693120 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 1573675X 13608185 |
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