首页> 中文期刊> 《湖南中医药大学学报》 >妇科千金片对盆腔炎大鼠TLR2/4-NF-κB信号通路影响的研究

妇科千金片对盆腔炎大鼠TLR2/4-NF-κB信号通路影响的研究

         

摘要

目的:观察妇科千金片对盆腔炎大鼠子宫 Toll 样受体2( TLR2)、Toll 样受体4( TLR4)、核转录因子 kappaB ( NF-κB ) mRNA 表达的影响,探讨妇科千金片调控 TLR2/4-NF-κB 信号通路对盆腔炎大鼠的抗炎机制。方法通过子宫注射混合菌液建立盆腔炎大鼠模型,将60只雌性 SD 大鼠随机分为5组,每组12只,即:空白组、假手术组、模型组、妇科千金片组、罗红霉素组,分别予以相应药物干预,运用免疫组化检测子宫组织中 TLR2、TLR4、NF-κB 的灰度值;运用实时荧光定量 PCR 检测子宫组织中 TLR2、TLR4、NF-κB 的 mRNA 表达变化。结果与空白组、假手术组比较,模型组的 TLR2、TLR4、NF-κB 灰度值显著降低( P<0.01), TLR2、TLR4、NF-κBmRNA 的表达均显著升高( P<0.01),表明模型成功;与模型组比较,妇科千金片组、罗红霉素组 TLR2、TLR4、NF-κB 灰度值均显著升高( P<0.01), TLR2、TLR4、NF-κBmRNA 均显著降低( P<0.01)。结论妇科千金片对盆腔炎大鼠抗炎的作用机制,可能是通过调控 TLR2/4-NF-κB 炎性介质变化信号通路的传导而实现的。%Objective To observe the effect of Fuke Qianjin tablets on the expression of TLR2, TLR4, NF-κB in pelvic inflammatory model rats, and to investigate its anti-inflammatory mechanism of TLR2/4-NF-κB signaling pathway on the pelvic inflammatory rats. Methods The 60 female SD rats were injected with the mixture of the uterus to establish the model of the rats with pelvic inflammatory disease. Then the rats were randomly divided into 5 groups, 12 rats in each group, namely: blank group, sham operation group, model group, Fuke Qianjin tablets group, roxithromycin group, which were given corresponding drug intervention. The gray values of TLR2, TLR4, NF-κB were detected by immunohistochemistry, and the expression of TLR2,TLR4, NF-κB mRNA of uterus was detected by real-time fluorescence quantitative PCR. Results Compared with the blank group, sham operation group, the gray values of TLR2, TLR4 and NF-κB in model group were decreased significantly (P<0.01), the expression of TLR2, TLR4 and NF-κB mRNA were significantly increased (P<0.01). Compared with the model group, the gray values of TLR2, TLR4 and NF-κB in Fuke Qianjin tablets group and roxithromycin group were significantly increased (P<0.01), the TLR2, TLR4 and NF-κB mRNA were significantly lower (P<0.01). Conclusion Mechanism of anti-inflammation of Fukeqianjin tablets on pelvic inflammatory model rats may be through the regulation of TLR2/4-NF-κB inflammatory medium signaling pathway.

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