摘要
目的观察地塞米松(DEX)对足细胞nephrin、Akt磷酸化及成纤维细胞特异性蛋白-1(fibroblast-specific protein1,FSP1)、结蛋白(desmin)表达的影响,探讨DEX在足细胞上皮间质转分化的可能作用。方法体外培养小鼠永生化足细胞,分别给予LPS或DEX干预,Annexin V-FITC/PI标记流式细胞测定足细胞的凋亡百分率,噻唑蓝(MTT)法测定足细胞活力,Western blot分别检测足细胞nephrin、Akt磷酸化水平,FSP1和desmin蛋白的表达。结果 LPS诱导足细胞凋亡,降低足细胞活力,减少nephrin、Akt的磷酸化,上调FSP1、desmin的表达;而DEX明显减少足细胞的凋亡,增加足细胞的活力,上调nephrin、Akt的磷酸化水平,降低FSP1、desmin的表达。结论地塞米松拮抗LPS引起的足细胞凋亡和失活,增加nephrin、Akt磷酸化水平,抑制足细胞上皮间质转分化而对足细胞有保护作用。
Objective To investigate the effect of dexamethasone （DEX） on the phosphorylation of nephrin and Akt, the expression of fibroblast - specific protein 1 （ FSP - 1 ） and desmin, and the possible role of DEX on podocyte epithelial - to - mesenchymal transdif- ferentiation（EMT）. Methods Immortalized mouse podocytes were treated with lipopolysaccharide（LPS） or DEX. The percentage of podocyte apoptosis was detected by flow cytometry with annexin V FITC/PI double staining. Podocyte viability was measured by using an MTT assay. The phosphorylation of nephrin and Akt and the expression of FSP - 1 and desmin proteins were detected by western blotting. Results LPS administration induced podocyte apoptosis, reduced podocyte viability, downregulated the expression of the phosphorylation of nephrin and Akt, upregulated the expression of FSP1 and desmin. DEX significantly reduced podocyte apoptosis, increased podocyte vi- ability, enchanced phosphorylation of nephrin and Akt, decreased the expression of FSP1 and desmin. Conclusion DEX reverses LPS - induced podocyte apoptosis and inactivation, and prevents the decline in phosphorylated nephrin and Akt in podocytes exposed to LPS, and inhibits podocyte EMT and has a protective effect on podocytes.
出处
《医学研究杂志》
2013年第11期127-130,共4页
Journal of Medical Research
关键词
地塞米松
脂多糖
足细胞
上皮间质转分化
Dexamethasone
Lipopolysaccharide
Podocyte
Epithelial - mesenchymal transdifferentiation
