| 张育,张学增,许金鑫,沈维干,高波.金雀异黄素对胶原诱导性关节炎大鼠成纤维样滑膜细胞MAPK信号通路的影响[J].,2011,31(10):1405-1408 |
| 金雀异黄素对胶原诱导性关节炎大鼠成纤维样滑膜细胞MAPK信号通路的影响 |
| Effect of Genistein on MAPK Signal Pathway in the Collagen-induced Arthritis Rat Fibroblast-like Synoviocytes |
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| DOI： |
| 中文关键词: 金雀异黄素 胶原诱导性关节炎 细胞外信号调节酶/磷酸化的细胞信号外节酶 成纤维样滑膜细胞 |
| 英文关键词:genistein collagen-induced arthritis collagen-induced arthritis extracellular signal-regulated kinase/phosphorylated extracellular signal-regulated kinase fibroblast-like synoviocyte |
| 基金项目:江苏省高校自然科学基础研究项目(No.07KJD320245) |
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| 中文摘要: |
| 目的研究金雀异黄素(genistein,Gen)对类风湿关节炎(rheumatoid arthritis,RA)动物模型胶原诱导性关节炎(collagen-induced arthritis,CIA)大鼠成纤维样滑膜细胞(fibroblast-like synoviocytes,FLS)MAPK信号传导通路的影响。方法建立CIA大鼠模型,将培养的CIA大鼠FLS采用随机法分组,采用四甲基偶氮唑盐(MTT)法检测Gen(浓度分别为50、100、200μmol/L)对CIA大鼠FLS增殖的影响;采用免疫印迹(Western blot)法检测Gen(浓度分别为50、100、200μmol/L)对CIA大鼠FLS细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)和磷酸化的细胞外信号调节激酶(phosphorylated extracellular signal-regulated kinase,p-ERK)表达的影响。结果 Gen能够抑制CIA大鼠FLS的增殖,Gen高剂量组细胞增殖度在72h仅为1.10±0.04,明显低于模型组2.12±0.03(P<0.01),并且Gen作用于FLS细胞后,p-ERK表达降低,Gen高剂量组仅为0.34±0.02,明显低于模型组2.68±0.14(P<0.01),而ERK表达无改变(P>0.05)。结论 Gen能够抑制CIA大鼠FLS的增殖,其作用机制主要与下调MAPK信号传导通路的酪氨酸激酶,抑制ERK的磷酸化有关。 |
| 英文摘要: |
| Objective To study the effect of genistein(Gen) on MAPK signal pathway in the CIA rat fibroblast-like synoviocytes(FLS).Methods The rat model of collagen-induced arthritis(CIA) was established.The cultured FLS of CIA rats were divided using randomized method.The effects of Gen(at the concentration of 50,100,and 200 μmol/L,respectively) on the proliferation of FLS in CIA rats using methyl thiazolyl tetrazolium(MTT) assay.Effects of Gen(at the concentration of 50,100,and 200 μmol/L,respectively) on the expressions of extracellular signal-regulated kinase(ERK) and phosphorylated extracellular signal-regulated kinase(p-ERK) in the FLS of CIA rats were detected.Results Gen could inhibit the proliferation of FLS in CIA rats.The FLS proliferation in the high dose Gen group at 72 h was only 1.10± 0.04,significantly lower than that in the model group(2.12±0.03,P<0.01).Besides,after Gen’s action on FLS,the expression of p-ERK was down-regulated.It was only 0.34±0.02 in the high dose Gen group,significantly lower than that in the model group(2.68±0.14,P<0.01).There was no change in the expression of ERK(P>0.05).Conclusions Gen could inhibit the proliferation of FLS in CIA rats.Its mechanism of action was mainly correlated to down-regulating the tyrosine kinase of MAPK signal transduction pathway and inhibiting phosphorylation of ERK. |
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