| 郭亚春,高亚贤,宋鸿儒.薯蓣皂苷片含药血清对IL-17和TNF-α诱导大鼠滑膜细胞株RSC-364 NF-κB p65、STAT3及VEGF影响的实验研究[J].,2013,33(6):0814-0818 |
| 薯蓣皂苷片含药血清对IL-17和TNF-α诱导大鼠滑膜细胞株RSC-364 NF-κB p65、STAT3及VEGF影响的实验研究 |
| Effects of Dioscornin Tablet Containing Serum on NF-κB p65， STAT3， and VEGF mRNA Expressions in Rats′ Synovial Cell Strain RSC-364 Induced by IL-17 and TNF-α |
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| DOI：10.7661/CJIM.2013.06.0814 |
| 中文关键词: 薯蓣皂苷片 类风湿关节炎 血管新生 核转录因子-κB p65 信号转导子和转录激活因子3 血管内皮生长因子 |
| 英文关键词:Dioscornin Tablet rheumatoid arthritis angiogenesis nuclear factor of kappa B p65 signal transducer and activator of transcription 3 vascular endothelial growth factor |
| 基金项目:国家自然科学基金资助项目（No30873420） |
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| 中文摘要: |
| 目的观察薯蓣皂苷片含药血清对白细胞介素-17（interieukin-17， IL-17）联合肿瘤坏死因子-α（tumor necrosis factor-α， TNF-α）诱导大鼠滑膜细胞株（rat synovial cell-364，RSC-364）核转录因子-κB （nuclear factor of kappa B，NF-κB）、信号转导子和转录激活因子3（signal transducer and activator of transcription 3， STAT3）及血管内皮生长因子（vascular endothelial growth factor， VEGF）表达的影响，探讨薯蓣皂苷片抑制类风湿关节炎 （rheumatoid arthritis，RA）血管新生可能的作用机制。方法实验设空白对照组、细胞模型组、薯蓣皂苷片含药血清组、雷公藤多苷片（阳性对照）含药血清组。制备薯蓣皂苷片和雷公藤多苷片含药血清；用IL-17和TNF-α联合刺激RSC-364建立RA细胞模型， 薯蓣皂苷片与雷公藤多苷片含药血清分别进行干预，应用TransAMTM NF-κB p65活性检测试剂盒检测NF-κB p65的DNA结合活性，应用Western blot方法观察STAT3蛋白的表达及应用实时荧光定量PCR方法观察VEGF mRNA表达。结果与空白对照组比较，IL-17和TNF-α联合诱导的细胞模型组核蛋白提取物中NF-κB p65DNA结合活性、STAT3蛋白表达及VEGF mRNA表达均显著增高（P<0.01，P<0.05）；与模型组比较，薯蓣皂苷片含药血清组、雷公藤多苷片含药血清组NF-κB p65的DNA结合活性、STAT3蛋白表达及VEGF mRNA表达均显著降低（P<0.01，P<0.05）。薯蓣皂苷片含药血清组与雷公藤多苷片含药血清组组间比较，差异无统计学意义（P>0.05）。结论薯蓣皂苷片可能通过抑制NF-κB信号转导通路中NF-κB p65的活性和酪氨酸蛋白激酶家族Janus kinase（JAK）－信号转导子和转录激活因子信号转导通路中STAT3蛋白表达来抑制VEGF mRNA表达，从而起到抑制RA血管新生的作用。 |
| 英文摘要: |
| ObjectiveTo observe the effects of Dioscornin Tablet （DT） containing serum on nuclear factor of kappa B （NF-κB） p65， signal transducer and activator of transcription 3 （STAT3）， and vascular endothelial growth factor （VEGF） mRNA expressions in rats′ synovial cell strain 364 （RSC-364） induced by interieukin-17 （IL-17） and tumor necrosis factor-α （TNF-α）， and to investigate the underlying mechanisms for DT to inhibit angiogenesis of rheumatoid arthritis （RA）. MethodsIn this experiment， the vehicle control group， the cell model group， the DT containing serum group， and the positive control group （Tripterygium containing serum） were set up. The DT containing serum and the Tripterygium containing serum were prepared. The RA cell model was established by IL-17 combined TNF-α induced injury in RSC-364. The RA cells were intervened by DT containing serum and Tripterygium containing serum respectively. The DNA binding activity of NF-κB p65 was detected using TransAMTM NF-κB p65. The expression of STAT3 was observed using Western blot. The VEGF mRNA expressions were detected by real-time quantitative PCR. ResultsCompared with the vehicle control group， the NF-κB p65 activity， the expressions of STAT3 and VEGF mRNA increased significantly in RSC-364 induced by IL-17+TNF-α （P<0.01， P<0.05）.
Compared with the model group， the NF-κB p65 activity， the expressions of STAT3 and VEGF mRNA decreased significantly in the DT containing serum group and the positive control group （P<0.01， P<0.05）. There was no statistical difference between the two groups （P>0.05）. ConclusionDT inhibited the VEGF mRNA expression through inhibiting the NF-κB p65 activity and the STAT3 protein expression in the Janus kinase （JAK）-signal transducer and activating transcription factor pathway， thus inhibiting the angiogenesis of RA. |
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