论文部分内容阅读
用IgG(10mg/ml)、不同浓度的牛血清白蛋白(BSA)(1,15,30mg/ml)和低密度脂蛋白(LDL100μg/ml)作用于体外培养的鼠肾小管上皮细胞株(NRK52E),采用流式细胞仪测定细胞表面CD40的平均荧光强度的变化。结果显示,BSA和IgG均不能引起细胞表面CD40表达的上调,与正常组相比,LDL100μg/ml可以刺激肾小管上皮细胞表达CD40的上调(P<0.05),提示CD40可能并不直接介导IgG和BSA造成的肾脏损害。低密度脂蛋白可以引起CD40的上调,提示异常蛋白负荷可能是造成病肾组织CD40上调的一个局部因素,异常蛋白负荷可能在CD40相关性肾炎中起一个促进的作用。
Rat renal tubular epithelial cell lines (NRK52E) cultured in vitro were treated with IgG (10 mg / ml), different concentrations of bovine serum albumin (BSA) (1,15,30 mg / ml) and low density lipoprotein (LDL 100 μg / ), The change of the average fluorescence intensity of CD40 on the cell surface was measured by flow cytometry. The results showed that both BSA and IgG could not upregulate the expression of CD40 on the cell surface. Compared with the normal group, LDL100μg / ml stimulated the up-regulation of CD40 expression in renal tubular epithelial cells (P <0.05), suggesting that CD40 may not directly mediate IgG And kidney damage caused by BSA. Low-density lipoprotein can cause upregulation of CD40, suggesting that abnormal protein load may be a local factor that leads to the upregulation of CD40 in diseased kidney. Abnormal protein load may play a promoting role in CD40-related nephritis.