Life sciences · 2011
Protective effect of telmisartan against cadmium-induced nephrotoxicity in mice.
Сравнительное исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Fouad Amr A, Jresat Iyad
Аннотация
AIMS: To investigate the nephroprotective effect of telmisartan, the angiotensin II receptor antagonist, against renal injury induced by cadmium in mice.
MAIN METHODS: Mice received cadmium chloride at a dose of 1.2mg Cd/kg/day, s.c., for nine weeks. Telmisartan treatment (1mg/kg/day, orally) was started one week before cadmium administration and continued for ten weeks.
KEY FINDINGS: Telmisartan significantly reduced blood urea nitrogen (BUN) and serum creatinine levels which were increased by cadmium. Also, telmisartan significantly suppressed lipid peroxidation, compensated deficits in the antioxidant defenses [reduced glutathione (GSH) level and catalase activity], decreased the elevations of tumor necrosis factor-α (TNF-α), nitric oxide (NO) and cadmium ion concentration, and attenuated the reductions of selenium and zinc ions in renal tissue resulted from cadmium administration. Histopathological examination revealed that cadmium-induced renal tissue damage was ameliorated by telmisartan treatment. Immunohistochemical analysis revealed that telmisartan significantly decreased the cadmium-induced overexpression of inducible nitric oxide synthase (iNOS), nuclear factor-κB (NF-κB), Fas ligand (FasL) and caspase-3 in renal tissue.
SIGNIFICANCE: Telmisartan, through its antioxidant and anti-inflammatory actions, effectively prevented cadmium nephrotoxicity in mice. Hence, telmisartan represents a potential candidate to protect the kidney from the detrimental effect of cadmium toxicity.
MAIN METHODS: Mice received cadmium chloride at a dose of 1.2mg Cd/kg/day, s.c., for nine weeks. Telmisartan treatment (1mg/kg/day, orally) was started one week before cadmium administration and continued for ten weeks.
KEY FINDINGS: Telmisartan significantly reduced blood urea nitrogen (BUN) and serum creatinine levels which were increased by cadmium. Also, telmisartan significantly suppressed lipid peroxidation, compensated deficits in the antioxidant defenses [reduced glutathione (GSH) level and catalase activity], decreased the elevations of tumor necrosis factor-α (TNF-α), nitric oxide (NO) and cadmium ion concentration, and attenuated the reductions of selenium and zinc ions in renal tissue resulted from cadmium administration. Histopathological examination revealed that cadmium-induced renal tissue damage was ameliorated by telmisartan treatment. Immunohistochemical analysis revealed that telmisartan significantly decreased the cadmium-induced overexpression of inducible nitric oxide synthase (iNOS), nuclear factor-κB (NF-κB), Fas ligand (FasL) and caspase-3 in renal tissue.
SIGNIFICANCE: Telmisartan, through its antioxidant and anti-inflammatory actions, effectively prevented cadmium nephrotoxicity in mice. Hence, telmisartan represents a potential candidate to protect the kidney from the detrimental effect of cadmium toxicity.
Предметные рубрики MeSH
Angiotensin Receptor AntagonistsAnimalsBenzimidazolesBenzoatesBlood Urea NitrogenCadmiumCatalaseCreatineFas Ligand ProteinGene Expression RegulationGlutathioneImmunohistochemistryKidneyKidney DiseasesLipid PeroxidationMiceNF-kappa BNitric OxideNitric Oxide Synthase Type IITelmisartanTumor Necrosis Factor-alpha