Immunohistochemical analysis of TGF-βand Smad in glomerular damage

1)不同肾小球损伤模型肾小球上皮细胞TGF-β和Smad表达的免疫组化研究在Wister大鼠中制作由抗Thy 1抗体诱导的系膜增生性GN模型、由嘌呤霉素氨基糖苷诱导的肾小球上皮细胞损伤模型、以及在WKY大鼠中制作由抗GBM抗体诱导的新月体形成模型，并且取出大鼠的肾脏并进行观察。在这些模型中，TGF-β1保持不变，但β2和β3在肾小球上皮细胞胞质中的表达增加。2）TGF- β和Smad在腹膜硬化性病变中表达的免疫组化研究硬化性腹膜炎是长期CAPD的并发症，应用免疫组化方法检测TGF-β在硬化性腹膜炎腹膜活检组织中的定位。TGF-β1、β2和β3在部分正常腹膜间皮细胞中呈弱阳性表达，其受体RI和R2在所有正常腹膜间皮细胞中均呈阳性表达。另一方面，在硬化性腹膜炎病例中观察到腹膜间皮细胞中TGF-β1、β2和β3的染色增加。β2和β3的表达特别强。在TGF-β的细胞内信号系统Smad家族中，Smad 4存在于正常腹膜的间皮细胞中。也有一些间皮瘤细胞，其中表达的抑制型Smad 6和Smad 7可以被证实。结论：抑制Smad家族（TGF-β的细胞内信号传导系统）可有效抑制TGF-β的作用，从而预防肾小球和腹膜病变。

1) Immunohistochemical study of the expression of TGF-β and Smad in glomerular epithelial cells of various glomerular injury models. A mesangial proliferative GN model induced by an anti-Thy 1 antibody, a glomerular epithelial cell injury model induced by Puromycin Aminonucleoside in Wister rats, and a crescentic formation model induced by an anti- GBM antibody in WKY rats were made, and kidneys of the rats were removed and observed. In these models, TGF-β1 remained unchanged, but the expression of β2 and β3 increased in the cytoplasm of glomerular epithelial cells. All the Smads were observed in the cytoplasm of these cells.2) Immunohistochemical study of the expression of TGF- β and Smad in peritoneal sclerotic lesions Sclerosing peritonitis is a complication associated with a long-term CAPD.Localization of TGF-βwas examined in peritoneal biopsy tissues of sclerotic peritonitis using an immunohistochemical method. While TGF-β1, β2 and β3 were stained slightly in some normal peritoneal mesothelial cells, their receptors RI and R2 were stained in all normal peritoneal mesothelial cells. On the other hand, increased staining of TGF-β1, β2 andβ3 in peritoneal mesothelial cells was observed in cases of sclerosing peritonitis. With the expression of β2 and β3 being particularly strong. In the Smad family, which is the intracellular signaling system of TGF-β, Smad 4 was found in the mesothelial cells of normal peritoneum. There were also some mesothelial cells in which expression of the inhibiting type of Smad 6 and Smad 7 could be confirmed. Conclusion : Suppression of the Smad family (the intracellular signaling system of TGF-β) may be effective for suppressing the action of TGF-β and thereby preventing glomerular and peritoneal lesions.