IgA nephropathy immortality compound particles on rat glomerulosclerosis TGF-β-Smads signal pathway.docVIP
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IgA nephropathy immortality compound particles on rat glomerulosclerosis TGF-β-Smads signal pathway
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IgA nephropathy immortality compound particles on rat glomerulosclerosis TGF-β/Smads signal pathway
Of: Huang Guodong, Xu Jian, Jiang Yun, Zhang Dandi Zhao Ying Sen
[Abstract] Objective To study the compound particles on IgA nephropathy of immortality (IgAN) glomerulosclerosis TGF-β/Smads signaling pathway in rats to investigate the mechanism of anti-renal fibrosis. Methods removal of the side of the kidney, repeated tail large intravenous dose of staphylococcal enterotoxin B (SEB) process to make closer to human IgAN glomerular sclerosis lesions in rats during the development of experimental animal models. The rats were randomly divided into normal control group, pathological model group, compound sen Treatment of grass group and Monnow treatment group, with the glomerular sclerosis index (GSI) Evaluation of drugs on renal glomerular sclerosis in IgAN pathological effects of immunohistochemical staining of renal tissue in each group compared TGF-β1, Smad2 and Smad7 protein expression differences. Results Compared with the control group, Group 3 rats were significantly glomerulus sclerosis, compared with model group, particle group and the compound of immortality hardening reduced significantly Monnow group, GSI has significant difference (P lt;0.01); immunohistochemical analysis of the pathological picture can be seen, compound immortality particle group and the Monnow group TGF-β1, Smad2 expression was significantly lower than model group (P lt;0.05 or lt;0.01), while Smad7 protein expression was significantly higher than the model (P lt;0.05 or lt;0.01), but the compound particle group and the Monnow immortality compared between groups, no significant difference (Pgt; 0.05). Conclusion The compound of immortality by reducing Smads2 protein particles, the increase Smad7 protein expression, thus inhibiting the over expression of TGF-β1, anti-IgAN glomerular sclerosis in rats continued progress, and this may be the important role o
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