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首页> 外文期刊>Cellular Physiology and Biochemistry >Isoliquiritigenin Inhibits Interferon-γ-Inducible Genes Expression in Hepatocytes through Down-Regulating Activation of JAK1/STAT1, IRF3/MyD88, ERK/MAPK, JNK/MAPK and PI3K/Akt Signaling Pathways
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Isoliquiritigenin Inhibits Interferon-γ-Inducible Genes Expression in Hepatocytes through Down-Regulating Activation of JAK1/STAT1, IRF3/MyD88, ERK/MAPK, JNK/MAPK and PI3K/Akt Signaling Pathways

机译：异智激肽原蛋白通过下调JAK1 / STAT1，IRF3 / MyD88，ERK / MAPK，JNK / MAPK和PI3K / Akt信号通路的激活抑制肝细胞中干扰素-γ诱导基因的表达

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Background & Aims: The high expression levels of interferon-γ (IFN-γ)-inducible genes correlate positively with liver diseases. The present study aimed to explore the effect of isoliquiritigenin (ISL) on the expression of genes induced by IFN-γ in vitro, and to elucidate the underlying molecular mechanisms. Methods: HepG2 and L02 cells were divided into control, ISL, IFN-γ, and IFN-γ plus ISL groups. The cytotoxicity of compounds to cells was evaluated by Cell Counting Kit 8 (CCK8) assay; the expression levels of chemokine (C-X-C motif) ligand 9 (CXCL9), CXCL10, CXCL11, and interleukin-6 (IL-6) in cells and supernatant were measured by quantitative real time polymerase chain reaction (qRT-PCR) and ELISA, respectively. Moreover, western blot was used to examine the phosphorylated levels of janus kinase (JAK)/signal transducer and activator of transcription 1 (STAT1), nuclear factor (NF)-κB, interferon regulatory factor 3 (IRF3)/myeloid differentiation factor 88 (MyD88), mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/Protein Kinase B (Akt) in HepG2 and L02 cells exposed to ISL, IFN-γ and IFN-γ plus ISL. Results: The results showed that IFN-γ treatment induced the expression of CXCL9, CXCL10, CXCL11, and IL-6 in HepG2 and LO2 cells, which could be significantly and dose-dependently inhibited by ISL treatment (P < 0.05 or P < 0.01), but the inhibitory effect of ISL on IL-6 expression was not so good as on CXCL9, CXCL10, and CXCL11 expression. Furthermore, ISL treatment dose-dependently inhibited the activation of JAK1/STAT1, IRF3/MyD88, extracellular signal-regulated kinase (ERK)/MAPK, c-Jun N-terminal kinase (JNK)/MAPK, and PI3K/Akt signaling pathways (P < 0.05), but had no effect on the activation of JAK2/STAT1, NF-κB and p38/MAPK signaling pathways. Conclusion: We demonstrate that ISL inhibits IFN-γ-induced inflammation in hepatocytes via influencing the activation of JAK1/STAT1, IRF3/MyD88, ERK/MAPK, JNK/MAPK, and PI3K/Akt signaling pathways.
机译：背景与目的：干扰素-γ（IFN-γ）诱导基因的高表达水平与肝脏疾病呈正相关。本研究旨在探讨异黄体生成素（ISL）对体外干扰素-γ诱导的基因表达的影响，并阐明其潜在的分子机制。方法：将HepG2和L02细胞分为对照组，ISL，IFN-γ和IFN-γ加ISL组。通过细胞计数试剂盒8（CCK8）分析评估了化合物对细胞的细胞毒性;通过定量实时聚合酶链反应（qRT-PCR）和ELISA分别测定趋化因子（CXC基序）配体9（CXCL9），CXCL10，CXCL11和白介素6（IL-6）在细胞和上清液中的表达水平。 。此外，western blot用于检查janus激酶（JAK）/信号转导子和转录激活因子1（STAT1），核因子（NF）-κB，干扰素调节因子3（IRF3）/髓样分化因子88的磷酸化水平（ MyD88），促分裂原激活蛋白激酶（MAPK），磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）在暴露于ISL，IFN-γ和IFN-γ加上ISL的HepG2和L02细胞中。结果：结果表明，IFN-γ处理可诱导HepG2和LO2细胞中CXCL9，CXCL10，CXCL11和IL-6的表达，ISL处理可显着且剂量依赖性地抑制其表达（P <0.05或P <0.01 ），但ISL对IL-6表达的抑制作用不如对CXCL9，CXCL10和CXCL11的抑制作用。此外，ISL治疗剂量依赖性地抑制JAK1 / STAT1，IRF3 / MyD88，细胞外信号调节激酶（ERK）/ MAPK，c-Jun N端激酶（JNK）/ MAPK和PI3K / Akt信号通路的激活（ P <0.05），但对JAK2 / STAT1，NF-κB和p38 / MAPK信号通路的激活没有影响。结论：我们证明ISL通过影响JAK1 / STAT1，IRF3 / MyD88，ERK / MAPK，JNK / MAPK和PI3K / Akt信号通路的激活来抑制IFN-γ诱导的肝细胞炎症。

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