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Role of N-acetylcysteine in protecting rats against contrast-induced acute kidney injury / 中华老年心脑血管病杂志
Chinese Journal of Geriatric Heart Brain and Vessel Diseases ; (12): 964-967, 2015.
Artigo em Chinês | WPRIM | ID: wpr-481176
ABSTRACT
Objective To study the role of N‐acetylcysteine (NAC) in protecting rats against con‐trast‐induced acute kidney injury .Methods Forty‐five adult Wistar rats were randomly divided into control group ,model group and NAC group (15 in each group) .Their serum levels of creati‐nine ,CRP ,TNF‐a were measured before ,and 48 and 72 h after contrast medium injection .The an‐imals were killed 72 h after contrast medum injection .Their serum levels of malondialdehyde , SOD ,NO were measured .Eexpressions of Bax and Bcl‐2 were detected .Results The serum levels of creatinine ,CRP ,TNF‐a ,malondialdehyde and the expression level of Bax were significantly higher in model group and NAC group than in control group ,and in model group than in NAC group after contrast injection (P< 0 .05) .The serum levels of SOD and NO and the expression level of Bcl‐2 were significantly lower in model group and NAC group than in control group ,and in model group than in NAC group after constrast injection (P< 0 .05) .Immunohistochemistry demonstrated that the TGFβ1 expression level was significantly higher in model group and NAC group than in control group and was significantly lower in NAC group than in model group .Con‐clusion NAC can protect rats against kidney injury and reduce contrast‐induced acute kidney in‐jury by inhibiting inflammation ,oxidation ,apoptosis and cytokines .

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Chinese Journal of Geriatric Heart Brain and Vessel Diseases Ano de publicação: 2015 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Chinese Journal of Geriatric Heart Brain and Vessel Diseases Ano de publicação: 2015 Tipo de documento: Artigo