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Angiotensin II receptor blockage prevents diabetes-induced oxidative damage in rat heart
Ozdemir S, Tandogan B, Ulusu NN, Turan B.
Jazyk angličtina Země Česko
NLK
Free Medical Journals
od 2000
Freely Accessible Science Journals
od 2000
ProQuest Central
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
- MeSH
- antagonisté receptorů pro angiotenzin MeSH
- benzimidazoly MeSH
- bifenylové sloučeniny MeSH
- blokátory receptorů AT1 pro angiotensin II farmakologie MeSH
- experimentální diabetes mellitus patofyziologie MeSH
- financování organizované MeSH
- glukosa-6-fosfátdehydrogenasa metabolismus MeSH
- glutathionperoxidasa metabolismus MeSH
- glutathionreduktasa metabolismus MeSH
- glutathiontransferasa metabolismus MeSH
- katalasa metabolismus MeSH
- krysa rodu rattus MeSH
- oxidační stres účinky záření MeSH
- potkani Wistar MeSH
- receptory angiotensinu MeSH
- tetrazoly farmakologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
Current findings suggest a role for the angiotensin II (Ang II) signalling pathway in generation of reactive oxygen species and diabetes-induced cardiac complications. In this study we aimed to investigate the effect of angiotensin II type 1 (AT1) receptor blockage on some antioxidant enzymes such as glucose- 6-phosphate dehydrogenase (G6PD), 6-phoshogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px), and catalase (CAT) in the heart of streptozotocin (STZ)-induced diabetic rats. The effect of AT1 receptor blocker, candesartan-cilexetil (5 mg/kg/day for 4 weeks) was studied. Diabetes caused hyperglycaemia (4-fold of control) with significant increases in G6PD, 6PGD, GR, GSH-PX, CAT and no effect on GST in heart tissues as compared to normal control rats. Treatment of STZ-induced diabetic rats with candesartan-cilexetil had significant beneficial effects on these parameters without any side effect on control rats. These results suggest that Ang II can take part in induction of oxidative stress in diabetic rat heart and that blockage of its activity by AT1 receptor blocker is potentially protective against diabetes-induced cellular damage.
Lit.: 36
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- $a Current findings suggest a role for the angiotensin II (Ang II) signalling pathway in generation of reactive oxygen species and diabetes-induced cardiac complications. In this study we aimed to investigate the effect of angiotensin II type 1 (AT1) receptor blockage on some antioxidant enzymes such as glucose- 6-phosphate dehydrogenase (G6PD), 6-phoshogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px), and catalase (CAT) in the heart of streptozotocin (STZ)-induced diabetic rats. The effect of AT1 receptor blocker, candesartan-cilexetil (5 mg/kg/day for 4 weeks) was studied. Diabetes caused hyperglycaemia (4-fold of control) with significant increases in G6PD, 6PGD, GR, GSH-PX, CAT and no effect on GST in heart tissues as compared to normal control rats. Treatment of STZ-induced diabetic rats with candesartan-cilexetil had significant beneficial effects on these parameters without any side effect on control rats. These results suggest that Ang II can take part in induction of oxidative stress in diabetic rat heart and that blockage of its activity by AT1 receptor blocker is potentially protective against diabetes-induced cellular damage.
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