Azilsartan improves glycemic status and reduces kidney damage in zucker diabetic fatty rats
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24598210
DOI
10.1093/ajh/hpu016
PII: hpu016
Knihovny.cz E-zdroje
- Klíčová slova
- azilsartan medoxomil, blood pressure, hypertension, inflammation, kidney injury, oxidative stress, type 2 diabetes.,
- MeSH
- benzimidazoly terapeutické užití MeSH
- blokátory receptorů AT1 pro angiotensin II terapeutické užití MeSH
- cévní endotel účinky léků MeSH
- diabetické nefropatie patologie prevence a kontrola MeSH
- glukózový toleranční test MeSH
- hyperglykemie farmakoterapie MeSH
- krevní glukóza metabolismus MeSH
- krevní tlak účinky léků MeSH
- krysa rodu Rattus MeSH
- oxadiazoly terapeutické užití MeSH
- oxidační stres účinky léků MeSH
- porucha glukózové tolerance prevence a kontrola MeSH
- potkani Zucker MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- azilsartan MeSH Prohlížeč
- benzimidazoly MeSH
- blokátory receptorů AT1 pro angiotensin II MeSH
- krevní glukóza MeSH
- oxadiazoly MeSH
BACKGROUND: Azilsartan medoxomil (AZL-M), an angiotensin II receptor blocker, demonstrates antihypertensive and organ protective effects in hypertension. We investigated the efficacy of AZL-M to ameliorate metabolic syndrome and kidney damage associated with type 2 diabetes using Zucker diabetic fatty (ZDF) rats. METHODS: ZDF rats were treated with vehicle or AZL-M for 8 weeks. Zucker diabetic lean (ZDL) rats were used as controls. Urine and plasma samples were collected for biochemical analysis, and kidney tissues were used for histopathological and immunohistopathological examination at the end of the 8-week protocol. RESULTS: ZDF rats were diabetic with hyperglycemia and impaired glucose tolerance, and AZL-M ameliorated the diabetic phenotype. ZDF rats were hypertensive compared with ZDL rats (181±6 vs. 129±7mm Hg), and AZL-M decreased blood pressure in ZDF rats (116±7mm Hg). In ZDF rats, there was marked renal damage with elevated proteinuria, albuminuria, nephrinuria, 2-4-fold higher tubular cast formation, and glomerular injury compared with ZDL rats. AZL-M treatment reduced renal damage in ZDF rats. ZDF rats demonstrated renal inflammation and oxidative stress with elevated urinary monocyte chemoattractant protein 1 excretion, renal infiltration of macrophages, and elevated kidney malondialdehyde levels. AZL-M reduced oxidative stress and inflammation in ZDF rats. CONCLUSIONS: Overall, we demonstrate that AZL-M attenuates kidney damage in type 2 diabetes. We further demonstrate that anti-inflammatory and antioxidative activities of AZL-M contribute to its kidney protective action.
Citace poskytuje Crossref.org
