Rationale

Ursolic acid (UA) has exhibited anti-inflammatory and anti-oxidative drug effects.

Objectives

In the research, we assessed the effects of UA on Nthy-ori 3-1 cells stimulated by IL-1β and attempted to elucidate the mechanisms underlying the effects.

Methods

Autoimmune thyroiditis (AIT) was simulated using Nthy-ori 3-1 cells by IL-1β (10 μM) treatment. UA (20 μM) was applied to ameliorate the injury of Nthy-ori 3-1 cells. The target of UA was predicted by TCMSP, BATMAN, and GEO database. Targeted relationship between lncRNA MALAT1 and miR-206, as well as miR-206 and PTGS1, was predicted by bioinformatics software and identified by dual luciferase assays. Cytokines in the cell supernatant and the apoptosis of cells were detected by ELISAs and flow cytometry assays, respectively. Expression levels of NF-κB signaling pathway-related proteins were estimated by western blot.

Results

By enquiring TCMSP, BATMAN, and GEO database, PTGS1 was identified as a target of UA. Afterward, a ceRNA network among MALAT1, miR-206, and PTGS1 was constructed. The expression levels of MALAT1 and PTGS1 in AIT tissues were obviously enhanced. Moreover, the ceRNA network formed by MALAT1/miR-206/PTGS1 contributed to the damage of Nthy-ori 3-1 cells induced by IL-1β. However, UA ameliorated the Nthy-ori 3-1 cells injury induced by IL-1β through mediating the MALAT1/miR-206/PTGS1 ceRNA network and NF-κB signaling pathway.

Conclusions

UA treatment significantly relieved the injury of Nthy-ori 3-1 cells via inhibiting the ceRNA mechanism of MALAT1/miR-206/PTGS1 and inflammatory pathways, insinuating that UA may be helpful for the treatment of AIT.

中文翻译：

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熊果酸通过限制 MALAT1/miR-206/PTGS1 ceRNA 网络和 NF-κB 信号通路改善 IL-1β 诱导的 Nthy-ori 3-1 细胞损伤

 基本原理

熊果酸（UA）具有抗炎和抗氧化药物作用。

 目标

在这项研究中，我们评估了 UA 对 IL-1β 刺激的 Nthy-ori 3-1 细胞的影响，并试图阐明其影响的机制。

 方法

使用 Nthy-ori 3-1 细胞通过 IL-1β (10 μM) 处理模拟自身免疫性甲状腺炎 (AIT)。应用UA (20 μM) 来改善Nthy-ori 3-1 细胞的损伤。通过TCMSP、BATMAN和GEO数据库预测UA的目标。通过生物信息学软件预测并通过双荧光素酶测定鉴定 lncRNA MALAT1 和 miR-206 以及 miR-206 和 PTGS1 之间的靶向关系。分别通过ELISA和流式细胞术检测细胞上清中的细胞因子和细胞凋亡。通过蛋白质印迹评估 NF-κB 信号通路相关蛋白的表达水平。

 结果

通过查询TCMSP、BATMAN和GEO数据库，确定PTGS1为UA的目标。随后，构建了 MALAT1、miR-206 和 PTGS1 之间的 ceRNA 网络。 AIT组织中MALAT1和PTGS1的表达水平明显增强。此外，MALAT1/miR-206/PTGS1形成的ceRNA网络有助于IL-1β诱导的Nthy-ori 3-1细胞损伤。然而，UA通过介导MALAT1/miR-206/PTGS1 ceRNA网络和NF-κB信号通路改善IL-1β诱导的Nthy-ori 3-1细胞损伤。

 结论

UA治疗通过抑制MALAT1/miR-206/PTGS1的ceRNA机制和炎症通路，显着减轻Nthy-ori 3-1细胞的损伤，暗示UA可能有助于AIT的治疗。