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Atorvastatin prevents gentamicin-induced renal damage in rats through the inhibition of p38-MAPK and NF-kappaB pathways.

dc.contributor.authorOzbek, Emin
dc.contributor.authorCekmen, Mustafa
dc.contributor.authorIlbey, Yusuf Ozlem
dc.contributor.authorSimsek, Abdulmuttalip
dc.contributor.authorPolat, Emre Can
dc.contributor.authorSomay, Adnan
dc.date.accessioned2023-05-16T17:06:16Z
dc.date.available2023-05-16T17:06:16Z
dc.description.abstractGentamicin (GM) is still considered to be an important antibiotic against life-threatening, gram-negative bacterial infections despite its known nephrotoxic effects. We aimed to evaluate the potential protective effect of atorvastatin (ATO) against GM-induced nephrotoxicity in rats.
dc.description.abstractThe rats were randomly divided into five groups of six animals each: control, GM (100 mg/kg/day), ATO (10 mg/kg/day), GM + ATO, and GM + Vehicle. Kidney function tests, tissue oxidative stress parameters, and histopathological and immunohistochemical studies clarified GM nephrotoxicity.
dc.description.abstractGM caused a marked reduction in renal functions and increased oxidative stress parameters. Histopathological examination revealed tubular necrosis especially in the renal cortex in GM rats. On immunohistochemical evaluation, GM rat showed more intense expressions of mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-kappaB), and inducible nitric oxide synthase (iNOS) compared with control. Kidney function tests and tissue oxidative stress parameters were normalized in the GM + ATO group. Histopathological and immunohistochemical pictures were also greatly ameliorated.
dc.description.abstractATO acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GM via the inhibition of MAPK and NF-kappaB signaling pathways and iNOS expression.
dc.identifier.pubmed19839839
dc.identifier.urihttps://hdl.handle.net/20.500.12645/38279
dc.language.isoen
dc.titleAtorvastatin prevents gentamicin-induced renal damage in rats through the inhibition of p38-MAPK and NF-kappaB pathways.
dspace.entity.typePublication
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