白芍总苷对糖尿病大鼠肾组织巨噬细胞TLR2与TLR4表达调节的研究

Effects of total glucosides of paeony on TLR2 and TLR4 expression in the kidney macrophages from diabetic rats

目的探讨白芍总苷对糖尿病大鼠肾组织巨噬细胞Toll样受体2与4表达的影响。方法建立链脲佐菌素诱导的大鼠糖尿病模型，将大鼠随机分对照组、模型组、白芍总苷给药组（50，100，200mg／kg／d灌胃）。8周后选用免疫组化单染及双染方法检验大鼠。肾组织巨噬细胞Toll样受体2、Toll样受体4以及核因子-kB-p-p65的表达。结果白芍总苷给药组（50，100，200mg／kg）鼠肾重／体质量以及尿蛋白水平明显低于模型组。白芍总苷给药组（50mg／kg）大鼠肾小球平均容量明显低于模型组，白芍总苷给药组（100与200mg／kg）平均容量与肾小管-间质损伤指数均明显低于模型组。模型组肾组织ED-1’细胞数明显高于对照组，白芍总苷给药组（50，100，200mg／kg）ED-1’细胞数较模型组明显下降，模型组。肾组织ED-1’Toll样受体2’、ED-1’Toll样受体4’以及核因子-kB-p-p65’细胞表达明显高于对照组，白芍总苷给药组（50，100，200mg／kg）肾组织中ED-1’Toll样受体2’、ED-I’Toll样受体4‘以及核因子-kBp-p65’细胞明显低于模型组。结论白芍总苷对于减少糖尿病大鼠早期肾脏损害有明显作用，其中与抑制糖尿病大鼠肾组织巨噬细胞Toll样受体2与4表达可能部分相关。

Objective To investigate regulation of total glucosides of paeony（TGP） on Toll-like-re- eeptor（TLR）2 and 4 in the kidney macrophage from diabetic rats. Methods Diabetes was induced by injec- tion of streptozotocin in rats. Rats were randomly divided into three groups： control group,model group,mod- el group treated with total glucosides of paeony. Total glucosides of paeony 50,100,200 mg/kg/d was orally administered once a day for 8 week. ED-1＋ ,ED-1＋ TLR2＋ ,ED-1＋ TLR4＋ and NF-kB-p-p65 ＋ cells were measured with immunohistochemistry and double immunohistochemistry. Results Kidney weight/body weight and AER was significantly lower in TGP treatment group than in model group. Elevated glomemlar volume was significantly attenuated by TGP treatment with 50,100 and 200 m_g/kg, and increased indices for tubulointerstitial injury were only ameliorated by TGP treatment with 100 and 200 mg/kg. There were marked accumulation of ED-1 ＋ cells in diabetic kidney, which were significantly inhibited by treatment with TGP, ED-1 ＋ TLR2 cells,ED-1 ＋ TLR4 cells and NF-kB-p-p65 ＋ cells were significantly elevated in the kid- neys from diabetic group,while they were significantly inhibited by TGP treatment. Conclusions TGP could ameliorate early renal injury and its mechanism may be at least partly correlated with the suppression of in- creased TLR2 and TLR4 expression in macrophages from diabetic rat kidney.