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Qing Hua Chang Yin inhibits the LPS-induced activation of the IL-6/STAT3 signaling pathway in human intestinal Caco-2 cells.
International Journal of Molecular Medicine ( IF 5.4 ) Pub Date : 2015-01-31 , DOI: 10.3892/ijmm.2015.2083
Xiao Ke 1 , Guanghong Hu 1 , Wenyi Fang 1 , Jintuan Chen 1 , Xin Zhang 1 , Chunbo Yang 1 , Jun Peng 2 , Youqin Chen 3 , Thomas J Sferra 3
Affiliation  

Increasing evidence indicates that the pathogenesis of ulcerative colitis (UC) is highly regulated by the interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) pathway and its negative feedback regulator, suppressor of cytokine signaling 3 (SOCS3). Therefore, modulating the signaling feedback loop of IL-6/STAT3/SOCS3 may prove to be a novel therapeutic approach for the treatment of UC. Qing Hua Chang Yin (QHCY) is a traditional Chinese formulation that has long been used in clinic for the treatment of UC. We have previously reported that QHCY ameliorates acute intestinal inflammation in vivo and in vitro through the suppression of the nuclear factor-κB (NF-κB) pathway. In the present study, in order to further elucidate the mechanisms responsible for the anti-inflammatory activities of QHCY, we stimulated human intestinal Caco-2 cells with lipopolysaccharide (LPS) to create an in vitro model of an inflamed human intestinal epithelium, and evaluated the effects of QHCY on the IL-6/STAT3/SOCS3 signaling network in inflamed Caco-2 cells. The levels of IL-6 were measured by ELISA and the levels of STAT3 and SOCS3 were measured by western blot analysis. We found that QHCY significantly inhibited the LPS-induced secretion of pro-inflammatory IL-6 in the Caco-2 cells in a dose-dependent manner. Moreover, QHCY profoundly suppressed the LPS-induced phosphorylation of Janus-activated kinase 1 (JAK1), JAK2 and STAT3. Furthermore, treatment with QHCY markedly augmented the expression of SOCS3. Taken together, the findings of the present study suggest that the modulation of the IL-6/STAT3/SOCS3 signaling network may be one of the mechanisms through which QHCY exerts its anti-inflammatory effects.

中文翻译:

清华肠饮抑制LPS诱导的人肠Caco-2细胞中IL-6 / STAT3信号通路的激活。

越来越多的证据表明,溃疡性结肠炎(UC)的发病机理受到白介素6(IL-6)/信号转导子和转录激活因子(STAT3)通路及其负反馈调节剂,细胞因子信号传导抑制因子3(SOCS3)的高度调控。 )。因此,调节IL-6 / STAT3 / SOCS3的信号反馈回路可能被证明是治疗UC的一种新颖的治疗方法。清华常饮(QHCY)是一种传统的中药配方,长期以来一直在临床上用于治疗UC。我们以前曾报道过,QHCY通过抑制核因子-κB(NF-κB)途径改善了体内和体外的急性肠道炎症。在本研究中,为了进一步阐明导致QHCY抗炎活性的机制,我们用脂多糖(LPS)刺激了人肠Caco-2细胞,以创建发炎人肠上皮的体外模型,并评估了QHCY对发炎Caco-2细胞中IL-6 / STAT3 / SOCS3信号网络的影响。通过ELISA测量IL-6的水平,并且通过western印迹分析测量STAT3和SOCS3的水平。我们发现,QHCY以剂量依赖性方式显着抑制Caco-2细胞中LPS诱导的促炎性IL-6分泌。此外,QHCY深刻抑制了LPS诱导的Janus激活激酶1(JAK1),JAK2和STAT3的磷酸化。此外,用QHCY处理显着增强了SOCS3的表达。在一起
更新日期:2019-11-01
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