Hong Lang1, Chun Dai2. 1. Department of Nephrology, Affiliated Hospital of Xuzhou Medical College, Hospital of Xuzhou Medical College, xuzhou, China. 2. Department of Nephrology, Affiliated Hospital of Xuzhou Medical College, Hospital of Xuzhou Medical College, xuzhou, China. Electronic address: 444085089@qq.com.
Abstract
BACKGROUND AND AIMS: We undertook this study to observe the effects of bone marrow mesenchymal stem cells (BMSCs) on plasminogen activator inhibitor-1 (PAI-1) and renal fibrosis in rats with diabetic nephropathy and to explore its main mechanism. METHODS: Thirty male Sprague Dawley rats were randomly divided into three groups: normal control group (NC group, n = 10), diabetic nephropathy group (DN group, n = 10), stem cell transplantation group (MSC group, n = 10). BMSCs were transplanted to rats in the MSC group via caudal vein infusion (2 × 10(6)/mL). At the end of 12 weeks, blood glucose, 24-h urinary protein, serum creatinine and renal mass index were measured. Morphology and collagen deposition in rat kidney were observed by HE and Masson staining, respectively. Expressions of PAI-1, transforming growth factor β1 (TGF-β1) and Smad3 in rat kidney were detected by immunohistochemistry and Western blot. RESULTS: Compared with DN group, 24-h protein, serum creatinine and renal mass index decreased significantly in MSC group. No significant changes in blood glucose (p >0.05) were shown. Immunohistochemistry and Western blot showed that expressions of PAI-1, TGF-β1 and Smad3 in NC group were lower than DN group. Expression of each protein in MSC group was between two groups (p <0.05). Correlation analysis revealed that PAI-1 and TGF-β1 (r = 0.987, p <0.05) and Smad3 (r = 0.974, p <0.05) showed a significant positive correlation. TGF-β1 and Smad3 (r = 0.962, p <0.05) were positively correlated. CONCLUSIONS: BMSCs significantly inhibited renal fibrosis in rats with DN. The mechanism may be related to inhibition of TGF-β1/Smad3 pathway, decreasing the expression of PAI-1 protein and reducing the accumulation of extracellular matrix, thereby balancing the fibrinolytic system.
BACKGROUND AND AIMS: We undertook this study to observe the effects of bone marrow mesenchymal stem cells (BMSCs) on plasminogen activator inhibitor-1 (PAI-1) and renal fibrosis in rats with diabetic nephropathy and to explore its main mechanism. METHODS: Thirty male Sprague Dawley rats were randomly divided into three groups: normal control group (NC group, n = 10), diabetic nephropathy group (DN group, n = 10), stem cell transplantation group (MSC group, n = 10). BMSCs were transplanted to rats in the MSC group via caudal vein infusion (2 × 10(6)/mL). At the end of 12 weeks, blood glucose, 24-h urinary protein, serum creatinine and renal mass index were measured. Morphology and collagen deposition in rat kidney were observed by HE and Masson staining, respectively. Expressions of PAI-1, transforming growth factor β1 (TGF-β1) and Smad3 in rat kidney were detected by immunohistochemistry and Western blot. RESULTS: Compared with DN group, 24-h protein, serum creatinine and renal mass index decreased significantly in MSC group. No significant changes in blood glucose (p >0.05) were shown. Immunohistochemistry and Western blot showed that expressions of PAI-1, TGF-β1 and Smad3 in NC group were lower than DN group. Expression of each protein in MSC group was between two groups (p <0.05). Correlation analysis revealed that PAI-1 and TGF-β1 (r = 0.987, p <0.05) and Smad3 (r = 0.974, p <0.05) showed a significant positive correlation. TGF-β1 and Smad3 (r = 0.962, p <0.05) were positively correlated. CONCLUSIONS: BMSCs significantly inhibited renal fibrosis in rats with DN. The mechanism may be related to inhibition of TGF-β1/Smad3 pathway, decreasing the expression of PAI-1 protein and reducing the accumulation of extracellular matrix, thereby balancing the fibrinolytic system.
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