Effect of rosiglitazone on the expression of fractalkine in renal cortex of type 2 diabetic rats

Abstract

Objective To investigate the effect of rosiglitazone on the expression of fractalkine in renal cortex of type 2 diabetic rats. Methods Thirty Sprague–Dawley (SD)rats were randomly divided into normal control group (n=10) and type 2 diabetic model groups which were induced by intraperitoneal injection of low–dose streptozotocin combined with high fat diet. After diabetes established, diabetic rats were then randomized to receive rosiglitazone (n=10) or vehicle (n=10) treatment. Serum advanced glycosylation end products–peptide (AGE–P) was measured by using flow injection assay. The mRNA and protein expressions of fractalkine were detected by semi–quantitative reverse transcription polymerase chain reaction and immunohistochemical staining, respectively. One–way analysis of variances was used for data analysis. Results The serum AGE–P[(2.87±0.21)U/ml], and the expression of fractalkine mRNA(1.41±0.03)and protein (0.79±0.04)in the renal cortex were significantly higher in the diabetes group than the normal control group [(0.90±0.13) U/ml, 0.85±0.04, and 0.46±0.03; P<0.01]. However, the serum AGE–P [(1.45±0.15) U/ml], and the expression of fractalkine mRNA (1.00±0.05) and protein (0.67±0.03) in the rosiglitazone group were significantly lower compared to the diabetes group (P<0.01). Conclusions Rosiglitazone may have renoprotective effects via inhibiting fractalkine expression in the renal cortex. Key words: Diabetic nephropathy; Glycosylation end products, advanced; Rosiglitazone; Fractalkine