Abstract:Objective To investigate the positions of Smad ubiquitin reglulator factor 2 (Smurf2) and transforming growth factor β1 (TGF-β1)expressions, their relation and the effects on renal lesions in rats with immunoglobulin (Ig)A nephropathy. Methods Twenty-seven male SD rats of 4-6 week old were randomly divided into three groups (n=9 each):normal control group, mild mesangial hyperplasia group and moderate-severe mesangial hyperplasia group. The IgA nephropathy model was established by the method of combined use of bovine serum (BSA), lipopolysaccharide (LPS) and carbon tetrachloride (CCl₄). Immunofluorescence in situ method was used to observe the location of Smurf2 and TGF-β1 proteins expressions. Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot were used to respectively detect the expressions of Smurf2, TGF-β1 mRNAs and proteins. Results IgA nephropathy model was established successfully. The degrees of mesangial hyperplasia and renal interstitial matrix hyperplasia and fibrosis in moderate-severe mesangial hyperplasia group were more obvious than those in mild mesangial hyperplasia group, while they were not found in normal control group. IgA granular-shape deposition was seen in mesangial region of IgA nephrotic group, and it was obvious in the middle and severe mesangial hyperplasia group, negative in the normal control group. The positions of Smurf2 and TGF-β1 proteins expressions were mainly in glomerulus, secondly in kidney tubules and occasionally in normal control group. The expression of Smurf2 protein was positively correlated with TGF-β1 protein. Both Smurf2 and TGF-β1 mRNAs expression levels in IgA nephropathy increased significantly compared with normal control group, and most of them were in moderate-severe mesangial hyperplasia group. Conclusion Both Smurf2 and TGF-β1 proteins expression positions were mainly in glomerulus and have same trend, namely, their expressions increased with the aggravation of mesangial hyperplasia degree. Increase of Smurf2 expression may play a role in promoting glomerulosclerosis and interstitial fibrosis in IgA nephropathy through exciting TGF-β1/Smad signaling pathway.