扶肾方对大鼠腹膜间皮细胞转分化的影响及机制探讨

Effect of Fushen Decoction on Transdifferentiation of Rat Peritoneal Mesothelial Cells and Its Mechanism

目的：观察扶肾方对腹膜透析大鼠腹膜间皮细胞转分化的影响及可能机制。方法：采用SD大鼠切除5/6肾脏＋1.5%百特腹透液的方法复制大鼠腹膜纤维化模型。扶肾方干预6周后,检测血清学指标肌酐和尿素氮的含量;HE观察腹膜形态的变化;RT-PCR法检测各组腹膜间充质标志物Vimentin和α-SMA的表达;ELASA法检测TGF-βRI和TGF-βRII含量的变化。结果：扶肾方干预后,各组血清肌酐及尿素氮均呈现下降趋势,尤其以高剂量组最为明显（P〈0.05）;扶肾方组腹膜间皮细胞变性、脱落,炎症细胞浸润以及血管新生现象明显减少;RT-PCR检测结果显示,与模型组相比,Vimentin各组表达均有所下降,但以中剂量组下调最为明显（P〈0.05）;腹膜纤维化相关因子TGF-βRI和TGF-βRII检测结果中,TGF-βRI的表达呈上升趋势,同模型组相比有显著性差异（P〈0.01,P〈0.05）,TGF-βRII的表达则呈下降趋势,差异有统计学意义（P〈0.05）。结论：扶肾方能够有效抑制腹膜间皮细胞转分化,改善腹膜纤维化,可能与调节TGF-βRI和TGF-βRII的表达有关。

Objective：To observe the effect of Fushen Decoction on peritoneal mesothelial cell transdifferentiation in peritoneal dialysis rats and its possible mechanism. Methods：Rat model of peritoneal fibrosis was induced by resection of SD rats 5/6 kidney＋ 1. 5% Baxter dialysis. After 6 weeks of intervention,the contents of creatinine and urea nitrogen were measured. The expressions of Vimentin and α-SMA were detected by RT-PCR. The changes of TGF-βRI and TGF-βRII were detected by ELASA. Results：The serum creatinine and urea nitrogen were decreased after the intervention of Fushen Formula,especially in high dose group（ P〈0.05）. Peritoneal mesothelial cell degeneration,inflammatory cell infiltration and angiogenesis were significantly reduced. The results of RT-PCR showed that the expression of Vimentin decreased compared with that of the model group,but the middle dose group＇s was the most significant（ P〈0.05）. The results of peritoneal fibrosis related factors TGF-βRI and TGF-βRII showed the expression of TGF-βRI was on the rise and had significant difference compared with that of the model group（P〈0.01,P〈0.05）. The expression of TGF-βRII had a downward trend and the difference was statistically significant（P〈0.05）. Conclusion：Fushen Decoction can effectively inhibit the transdifferentiation of peritoneal mesothelial cells and improve the peritoneal fibrosis,which may be related to the regulation of TGF-βRI and TGF-βRII.