Inhibition of intestinal ischemia/repurfusion induced apoptosis and necrosis via down-regulation of the NF-kB, c-Jun and caspace-3 expression by epigallocatechin-3-gallate administration
Autor: | Georgios Papageorgiou, D Takoudas, Nicholas Kontos, Konstantinos Atmatzidis, Alexandros Giakoustidis, Kokona Koliakou, Nickolaos Antoniadis, Stavros Iliadis, Vasilios Papanikolaou, Dimitrios Giakoustidis, Eleni Kaldrymidou |
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Rok vydání: | 2008 |
Předmět: |
Male
Necrosis Proto-Oncogene Proteins c-jun Down-Regulation Apoptosis Caspase 3 Biochemistry Catechin chemistry.chemical_compound Ischemia Malondialdehyde In Situ Nick-End Labeling medicine Animals Intestinal Mucosa Rats Wistar Peroxidase chemistry.chemical_classification Microscopy Reactive oxygen species TUNEL assay biology c-jun NF-kappa B General Medicine Molecular biology Rats Intestines chemistry Reperfusion Injury Myeloperoxidase biology.protein medicine.symptom |
Zdroj: | Free Radical Research. 42:180-188 |
ISSN: | 1029-2470 1071-5762 |
Popis: | Intestinal ischemia/reperfusion (I/R) produces reactive oxygen species (ROS) activating signal transduction and apoptosis. The aim of this study was to evaluate the effect of (-)-epigallocatechin-3-gallate (EGCG) administration in inhibition of apoptosis by attenuating the expression of NF-kB, c-Jun and caspace-3 in intestinal I/R. Thirty male wistar rats were used. Group A sham operation, B I/R, C I/R-EGCG 50 mg/kg ip. Intestinal ischemia was induced for 60 min by clamping the superior mesenteric artery. Malondialdehyde (MDA), myeloperoxidase (MPO), light histology, Fragment End Labelling of DNA (TUNEL), immunocytochemistry for NF-kB, c-Jun and caspace-3 analysis in intestinal specimens were performed 120 min after reperfusion. Apoptosis as indicated by TUNEL and Caspace-3, NF-kB and c-Jun was widely expressed in I/R group but only slightly expressed in EGCG treated groups. MDA and MPO showed a marked increase in the I/R group and a significant decrease in the EGCG treated group. Light histology showed preservation of architecture in the EGCG treated group. In conclusion, EGCG pre-treatment is likely to inhibit intestinal I/R-induced apoptosis by down-regulating the expression of NF-kB, c-Jun and caspase-3. |
Databáze: | OpenAIRE |
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