目的观察大黄酸(Rheic acid)对高糖(30mmol/L)诱导的大鼠肾脏系膜细胞(MsC)转化生长因子β1(TGF-β1)及单核细胞趋化因子(MCP-1)表达的影响,探讨其肾脏保护的可能机制。方法大黄酸作用于高糖诱导的MsC,运用MTS检测细胞存活率,ELISA法测定细胞上清TGF-β1、MCP-1含量,RT-PCR法检测MCP-1、TGF-β1 m RNA表达量。结果与模型组(高糖30mmol/L)比较,大黄酸(62.5、125、250μg/mL)干预组Ms C细胞存活率明显上升(59%、75%、84%比53%,P〈0.05)。高糖(30mmol/L)作用于Ms C细胞后,TGF-β1、MCP-1表达被激活,与正常组比较,差异有统计学意义(P〈0.05)。大黄酸(62.5、125、250μg/mL)干预后,TGF-β1及MCP-1活性均被抑制,与模型组比较,差异均有统计学意义(P〈0.05)。结论大黄酸可以通过调控MCP-1和TGF-β1表达,从而减少高糖诱导的MsC炎症反应。
Objective To investigate the effect of Rheic acid on the expression of transforming growth factor-βl(TGF-β1) and monocyte chemoattractant protein-1(MCP-1)on mesangial cells of high glucose(30mmol/L) induced diabetic rats and the mechanism under its renal protection. Methods Mesangial cells from diabetic rats induced by high glucose was treated with Rheic acid, then the cell survival rate was detected by using MTS method, the level of TGF-β1 and MCP-1in cell supernatant was determined with ELISA, and the m RNA transcription of MCP-1 and TGF-β1 was assessed by RT-PCR. Results Compared with model group(high glucose group), the cell survival rate in Rheic acid groups(62.5, 125, 250μg/mL) increased(84%, 75%, 59% vs 53%, all P〈0.05). The expression of TGF-β1 and MCP-1 in high glucose-induced mesangial cells was increased compared with healthy mesangial cells(P〈0.05), but the increase was significantly inhibited after the treatment of Rheic acid(62.5, 125,250μg/mL, all P〈0.05). Conclusion Rheic acid can alleviatehigh glucose-inducedinflammatoryresponse of mesangial cells by regulating the expression of TGF-β1 and MCP-1.