Study of glomerular podocyte injury induced by aristolochic acid
10.3760/cma.j.issn.1001-7097.2012.03.013
- VernacularTitle:马兜铃酸损伤大鼠肾小球足细胞的研究
- Author:
Hong CHENG
;
Yipu CHEN
;
Hongrui DONG
;
Yanyan WANG
;
Hongliang RUI
- Publication Type:Journal Article
- Keywords:
Aristolochic acid;
Podocyte;
Injury
- From:
Chinese Journal of Nephrology
2012;28(3):222-225
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore whether the glomerular podocytes can be damaged by aristolochic acid. Methods Thirty-two male SD rats were equally divided into the following 2 groups:model group in which the rats received the extract of Aristolochia manshuriensis Kom (AmK) by gavage; control group only received tap water by gavage.24 h urinary protein excretion was measured at the end of the 1st and 4th week,and SDS-PAGE gel electrophoresis was performed to detect the protein in urine.At the end of the 4th week,all the rats were sacrificed and the glomeruli were isolated by laser capture microdissection technique.The mRNA expression of nephrin,podocin,CDA2P,podocalyxin and podoplanin in isolated glomeruli was determined by RT-PCR,and the average width of glomerular foot process was measured by electron microscopy and image analysis. Results At the end of the 4th week,24 h urinary protein excretion in the model group was significantly higher than that in the control group (P<0.01) and the urinary albumin content in model group was also obviously increased.The average width of glomerular foot process in the model group was significantly larger than that in control group (P<0.01).The mRNA expressions of nephrin,podocin,CDA2P,podocalyxin and podoplanin in glomeruli were significantly down-regulated in the model group compared with the control group,which decreased by 34%,62%,56%,50%(P<0.01) and 27% (P<0.05),respectively. Conclusions Aristolochic acid can damage the glomerular podocytes,resulting in the down-regulation of nephrin,podocin,CD2AP,podoplanin and podocalyxin mRNA expression, the segmental widening of foot process, and increased urinary protein excretion.