Bone marrow mesenchymal stem cell transplantation for repair of mesangial proliferative glomerulonephritis:role and mechanism / 中国组织工程研究

ABSTRACT

BACKGROUND:Bone marrow mesenchymal stem cel s are likely to repair renal injury by differentiating into renal parenchymal cel s. OBJECTIVE:To explore the effect and mechanism of bone marrow mesenchymal stem cel s in the renal repair after mesangial proliferative glomerulonephritis. METHODS:Thirty Sprague-Dawley rats were randomized into normal group, model group and treatment group (n=10 per group). Model group and treatment group were treated with tail vein injection of mouse anti-rat monoclonal antibody Thy1.1 to prepare mesangial proliferative glomerulonephritis models. One week after modeling, rats in the treatment group were given 2×106 bone marrow mesenchymal stem cel s via the tail vein, and rats in the other two groups were given the same volume of normal saline. Two weeks after transplantation, urinary protein, urea nitrogen, creatinine levels were detected;hematoxylin-eosin staining was used for observing pathological changes of the renal tissue under microscope;and the expression of transforming growth factor beta 1 was detected by immunohistochemistry method. RESULTS AND CONCLUSION:The levels of urinary protein, urea nitrogen and creatinine as wel as the expression of transforming growth factor beta 1 in the renal tissue arranged in descending order were listed as fol owsmodel group>treatment group>control group, and there were significant differences among three groups (P<0.05). In the model group, diffuse glomerular hyperplasia was observed with the presence of increased extracel ular matrix, partial glomerular sclerosis, and interstitial infiltration of inflammatory cel s;in the treatment group, glomerular hyperplasia, mesangial proliferation and inflammatory cel infiltration were al mitigated compared with the model group. Therefore, bone marrow mesenchymal stem cel transplantation may contribute to renal repair after mesangial proliferative glomerulonephritis, by inhibiting overexpression of transforming growth factor beta 1 in the kidney.