Qing Hua Chang Yin inhibits the LPS-induced activation of the IL-6/STAT3 signaling pathway in human intestinal Caco-2 cells

SOCS3 车站3 STAT蛋白 信号转导 贾纳斯激酶 细胞因子信号抑制因子 细胞因子 肠上皮 生物 炎症 细胞生物学 Janus激酶2 癌症研究 化学 免疫学 上皮 遗传学
作者
Xiao Ke,Guanghong Hu,Wenyi Fang,Jin-tuan Chen,Xin Zhang,Chunbo Yang,Jun Peng,Youqin Chen,Thomas J. Sferra
出处
期刊:International Journal of Molecular Medicine [Spandidos Publications]
卷期号:35 (4): 1133-1137 被引量:11
标识
DOI:10.3892/ijmm.2015.2083
摘要

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.
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