Effect of prednisone on expression of Ezrin and NEPH1 in rats with Adriamycin-induced nephrosis
10.3760/cma.j.issn.2095-428X.2013.17.012
- VernacularTitle:Ezrin和NEPH1在多柔比星肾病大鼠肾组织中的表达及泼尼松对其表达的影响
- Author:
Juan WANG
1
;
Bi-Li ZHANG
Author Information
1. 300070,天津医科大学研究生院
- Keywords:
Adriamycin-induced nephrosis;
Nephrotic syndrome;
Prednisone;
Ezrin;
NEPH1
- From:
Chinese Journal of Applied Clinical Pediatrics
2013;28(17):1323-1326
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of proteinuria and renal protection of prednisone by observing the expressions of Ezrin and NEPH1 in rats with Adriamycin (ADR)-induced nephrosis.Methods The 24 rats were divided into 3 groups,which were control group,model group and prednisone group.ADR model was induced by a tail intravenous injection of ADR for 2 times.Serum index and 24 h urinary protein were measured in 4 and 8 weeks.The expressions of Ezrin and NEPH1 in glomerulus were evaluated by using two-step immunohistochemistry respectively.Results Compared with control group,heavy proteinuria,hypoalbuminemia,hyperlipemia were observed in 4 weeks in the model group and the prednisone group which indicated that the models were successfully established.Compared with model group,in 8 weeks,24 h urinary protein,total cholesterol and serum creatinine in prednisone group were significantly decreased(all P ＜ 0.0 l),while albumin,total protein and endogenous creatinine clearance rate were significantly increased(all P ＜ 0.05) ;The expressions of Ezrin and NEPH1 in model group were significantly decreased compared with control group(all P ＜ 0.01).The expressions of Ezrin and NEPH1 in prednisone group were significantly increased compared with model group(all P ＜0.01).The expressions of Ezrin and NEPH1 were negatively related to proteinuria(r =-0.838,-0.884,all P ＜ 0.01).Conclusions The declined expressions of Ezrin and NEPH1 in rats with ADR-induced nephrosis may be one of mechanisms of proteinuria.Prednisone can reduce the proteinuria and relieve the renal pathological damage by improving the expression of Ezrin and NEPH1.
