Expression of renal integrin-linked kinase and lesion of podocyte in a diet-induced hyperlipidemic model of rats
10.3760/cma.j.issn.1001-7097.2009.07.005
- VernacularTitle:高脂诱导大鼠肾组织整合素连接激酶表达及足细胞损害
- Author:
Xiaogang DU
;
Hua GAN
;
Zhimei LV
- Publication Type:Journal Article
- Keywords:
Hyperlipoidemia;
Podocyte;
Desmin;
Integrin-linked kinase
- From:
Chinese Journal of Nephrology
2009;25(7):514-518
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the lesion of podocyte and the expression of renal integrin-hnked kinase (ILK) in a diet-induced hyperlipidemic model of rats. Methods Thirty-six 6-8 week-old female Wistar rats were randomly assigned into three groups, high-fat diet group, rats in each group were sacrificed at the 4th and 10th week respectively. The levels of serum cholesterol and triglyceride were determined by enzymic method. The morphology of podocyte was observed and photographed with electron microscope. The expression of ILK mRNA was determined by RT-PCR. The expressions of ILK and desmin protein were determined by Western blot analysis. The distribution of ILK in renal tissue was examined by immunohistochemieal staining. Results Levels of serum cholesterol and triglyceride, the expression of desmin, renal ILK mRNA and protein, as well as the foot process effacement were significantly up-regulated in both high-fat diet group and simvastatin group as compared with control group. However, all of the above parameters were ameliorated in simvastatin group as compared with high-fat diet group (P<0.01). ILK was mainly expressed in glomendar podocytes and renal tubular cells by immunohistochemical staining, and its change was similar to the results detected by Western blot analysis in each group. A positive correlation was found between ILK protein expression and desmin expression in renal tissue(r=0.93107, R2=0.8669, P<0.01). Conclusions Podocyte lesion can be induced by high-fat diet, which is correlated with over-expression of renal ILK. Simvastatin may play an important role in protecting against podocyte injury induced by hyperlipoidemia, properly through down-regulating ILK expression in renal tissue.
