Mechanism of Nephrotoxicity of Aloe Emodin in Mice / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae
;
(24): 48-53, 2019.
Artículo
en Chino
| WPRIM
| ID: wpr-802197
ABSTRACT
Objective:
To study nephrotoxicity induced by long-term administration of different doses of aloe-emodin in mice, and explore its mechanism.Method:
A total of 30 male and female Kunming mice were randomly divided into normal control group, and low-dose aloe-emodin group,high-dose aloe-emodin group (0.8,1.6 g·kg-1). Every dose of group was administered intragastrically for 11 weeks,twice daily. effect of serum urea nitrogen (BUN),creatinine (SCr),superoxide dismutase (SOD),malondialdehyde (MDA),Glutathione (GSH/GSSG) and Glutathione Peroxidase (GSH-Px) levels were detected by biochemical kits according to manufacturer's instruction. Enzyme-linked immune assay was used to determine serum tumor necrosis factor (TNF)-α and interleukins(IL)-6 levels. Hematoxylin eosin (HE) staining was used to detect renal pathological changes in kidney tissues, and cysteine aspartic acid specific protease(Caspase)-3 and transforming growth factor(TGF)-β1 proteins were determined by immunohistochemistry.Result:
According to results,compared with normal control group,the levels of BUN and SCr in serum with high-dose aloe-emodin were increased. The renal tubules in low-dose group were mildly injured,while renal tubules and glomeruli of high-dose group were moderately damaged. Compared with normal control group,the level of SOD was significant decreased (PPPPα and IL-6 were increased,the expression of TGF-β1 protein in kidneys was increased in low-dose and high-dose groups (PConclusion:
results show that 1.6 g·kg-1 aloe-emodin was administered intragastrically for 11 weeks,which had toxic effects on kidney in mice. The mechanism may be related to oxidative stress,apoptosis and TGF-β1 protein expression.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Chinese Journal of Experimental Traditional Medical Formulae
Año:
2019
Tipo del documento:
Artículo
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