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首页> 外文期刊>Life sciences >Shikonin inhibited mitogen-activated IL-4 and IL-5 production on EL-4 cells through downregulation of GATA-3 and c-Maf induction.
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Shikonin inhibited mitogen-activated IL-4 and IL-5 production on EL-4 cells through downregulation of GATA-3 and c-Maf induction.

机译：Shikonin通过GATA-3和C-MAF诱导的下调抑制EL-4细胞上的丝裂剂活化的IL-4和IL-5产生。

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摘要

AIM: To investigate the effects of shikonin on phorbol myristate acetate (PMA) plus cyclic adenosine monophosphate (cAMP)-induced T helper (T(H)) 2 cell cytokine production, and the underlying mechanism. MAIN METHODS: We used activated EL-4 murine T-lymphoma cells, which produce interleukin (IL)-4 and IL-5, but not interferon (IFN)-gamma, as T(H)2 cell-like cells and treated them with PMA+cAMP to investigate the effects of shikonin on T(H)2 cytokines, transcriptional factors, and the related mitogen-activated protein kinase (MAPK)/nuclear factor (NF)-kappaB signaling pathway. KEY FINDINGS: The data show that shikonin inhibited the PMA+cAMP-induced mRNA and protein expression of IL-4 and IL-5 via the downregulation of GATA-binding protein-3 (GATA-3) and c-musculoaponeurotic fibrosarcoma (Maf) but not T-box expressed in T cells (T-bet). Moreover, shikonin suppressed the phosphorylation of p38, inhibitor of kappaB (IkappaB) kinase (IKK)-beta and IkappaB-alpha, and the subsequent IkappaB-alpha degradation induced by PMA+cAMP; however, the PMA+cAMP-induced phosphorylation of extracellular signal-related kinase (ERK), which resulted in minor inhibition and phosphorylation of c-Jun N-terminal kinase (JNK), seemed to be unaffected by shikonin treatment. SIGNIFICANCE: This study suggests that downregulation of GATA-3 and c-Maf via the suppression of p38, IKK-beta and IkappaB-alpha phosphorylation might contribute to the inhibitory effect of shikonin on mitogen-induced IL-4 and IL-5 production in EL-4T cells. Furthermore, shikonin is a potential drug for treating allergic diseases.
机译：目的：探讨Shikonin对醋酸氏植物的醋酸骨糖（PMA）加环腺苷一磷酸（CAMP）诱导的T辅助剂（T（H））2细胞细胞因子的产生和潜在机制。主要方法：我们使用激活的EL-4鼠T淋巴瘤细胞，其产生白细胞介素（IL）-4和IL-5，但不是干扰素（IFN）-γ，作为T（H）2细胞样细胞并处理它们用PMA +阵营探讨Shikonin对T（H）2细胞因子，转录因子和相关丝肠激活蛋白激酶（MAPK）/核因子（NF）信号传导途径的影响。主要发现：数据显示，世素蛋白通过GATA结合蛋白-3（GATA-3）和C-Musculaponecoric Fibrosarcoma（MAF）的下调抑制IL-4和IL-5的PMA + CAMP诱导的mRNA和蛋白表达但不是在T细胞（T-BET）中表达的T盒。此外，什耳素抑制了P38，κB抑制剂（Ikappab）激酶（IKK）-Beta和Ikappab-α的磷酸化，以及PMA + CAMP诱导的随后的Ikappab-α降解;然而，PMA + CAMP诱导的细胞外信号相关激酶（ERK）的磷酸化，导致C-JUM N-末端激酶（JNK）的轻微抑制和磷酸化，似乎不受欢迎的是Shikonin治疗。本研究表明，通过抑制P38，IKK-β和IKAPPAB-α磷酸化的降低GATA-3和C-MAF可能有助于Shikonin对丝裂诱导的IL-4和IL-5产生的抑制作用EL-4T细胞。此外，Shikonin是一种治疗过敏性疾病的潜在药物。

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