黄晓霞 柯昌斌 张庆红 李涛 张建鄂

　　作者单位：442000湖北十堰，湖北医药学院附属太和医院肾内科(黄晓霞、张庆红、李涛、张建鄂)，麻醉科(柯昌斌)

　　【摘要】目的 观察PI3K/Akt在高糖诱导的肾小管上皮细胞转分化中的作用及对分化抑制因子2(Id2)表达的影响。 方法 大鼠肾小管上皮细胞随机分成3组：对照(Con)组，高糖(H-Glu)组和PI3K抑制剂Wortmannin(Wort)组。Con组加正常培养液，H-Glu组在培养液中加30 mmol/L葡萄糖，Wort组用Wortmannin预处理1 h后，加30 mmol/L葡萄糖。24 h后用免疫细胞化学、Western blot法和RT-PCR法检测α平滑肌肌动蛋白(α-SMA)、p-Akt和Id2的表达。 结果 Con组α-SMA、p-Akt阳性表达细胞很少，绝大部分细胞出现Id2阳性表达。与Con组比较，H-Glu组出现α-SMA和p-Akt表达升高，Id2表达降低(P<0.05)。与H-Glu组比较，Wort组α-SMA 和p-Akt表达下降，Id2表达升高(P<0.05)。 结论 PI3K/Akt可能通过抑制Id2基因表达，参与高糖诱导的大鼠肾小管上皮细胞转分化。

　　【关键词】PI3K/Akt;分化抑制因子;肾小管上皮细胞;转分化

　　doi:10.3969/j.issn.1006-6187.2011.02.017

　　Role of PI3K/Akt pathway in tubular epithelial-myofibroblast transition induced by high glucose and its effects on inhibitor of differentiation 2 (Id2) expression

　　HUANG Xiao-xia, KE Chang-bin, ZHANG Qing-hong, et al. Department of Nephrology, Taihe Hospital of Hubei University of Medicine, Hubei Shiyan 442000, China

　　【Abstract】Objective To observe the effects of PI3K/Akt on inhibitor of differentiation 2 in tubular epithelial-myofibroblast transition induced by high glucose.MethodsNormal rat kidney tubular epithelial cells were randomly divided into three groups:control group(group Con),high glucose group (group H-Glu) and wortmannin group(group Wort). Cells in group Wort were pretreated with wortmannin for an hour before stimulation with high glucose ( 30mmol/L) in group H-Glu and Wort, and cells in group Con were treated with media only. Twenty four hours later, the level of phosphorylation Akt ,Id2 and expression of α-SMA were assayed.ResultsExpression of p-Akt and α-SMA were very low and most of the cell had positive expression of Id2 in group Con. In group H-Glu the expression of α-SMA and p-Akt increased and Id2 decreased significantly, while in group Wort the wortmannin obviously alleviated the change induced by high glucose.  Conclusions  PI3K/Akt may involve in tubular epithelial-myofibroblast transition induced by high glucose through inhibiting Id2.

　　【Key words】PI3K/Akt; Inhibitor of differentiation; Renal tubular epithelial cell; Transdifferentiation