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首页> 外文期刊>Drug Design, Development and Therapy >Triptolide Inhibits the Proliferation of HaCaT Cells Induced by IL22 via Upregulating miR-181b-5p
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Triptolide Inhibits the Proliferation of HaCaT Cells Induced by IL22 via Upregulating miR-181b-5p

机译：雷丝酮通过上调miR-181b-5p抑制IL22诱导的HACAT细胞的增殖

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Background: Evidence has been shown that triptolide was effective in the treatment of psoriasis; however, the mechanisms remain poorly understood. Thus, this study aimed to investigate the role of triptolide on the proliferation and differentiation of HaCaT cells which are treated with IL22 to mimic abnormal proliferation/differentiation in keratinocyte of psoriasis. Materials and Methods: HaCaT cells were transfected with miR-181b-5p antagomir for 24 h, and then exposed to 10 μM Triptolide for 24 h, following by 100 ng/mL of IL22 for 24 h. In addition, the proliferation and cell cycle distribution in HaCaT cells were assessed by immunofluorescence or flow cytometry assays, respectively. Results: Triptolide obviously upregulated the level of miR-181b-5p in HaCaT cells. In addition, triptolide significantly inhibited IL22-induced proliferation of HaCaT cells via inducing cell cycle arrest. Moreover, IL22 markedly inhibited the differentiation of HaCaT cells, and this phenomenon was reversed by triptolide treatment. In contrast, the effects of triptolide on the proliferation and differentiation in IL22-stimulated HaCaT cells were notably reversed by miR-181b-5p antagomir. Moreover, dual-luciferase assay showed that E2F5 was the direct target of miR-181b-5p in HaCaT cells. Meanwhile, upregulation of miR-181b-5p obviously decreased the level of E2F5 in HaCaT cells. Conclusion: In this study, we found that triptolide could inhibit the proliferation and promote the differentiation in IL22-stimulated keratinocytes via upregulating miR-181b-5p. These data indicated that triptolide may be a potential agent for the treatment of psoriasis.
机译：背景：已经表明证据表明，雷公藤内酯在治疗牛皮癣方面是有效的;然而，机制仍然明白。因此，该研究旨在探讨雷公藤内酯对蜂窝状细胞的增殖和分化的作用，该细胞用IL22处理，以模仿牛皮癣角质细胞的异常增殖/分化。材料和方法：用miR-181b-5p抗蛋白体转染24小时，然后暴露于10μm的胎冬叶片24小时，含100ng / ml Il 2 2 24小时。此外，通过免疫荧光或流式细胞术测定分别评估HACAT细胞中的增殖和细胞周期分布。结果：Triptolide明显上调了HaCAT细胞miR-181b-5p水平。此外，通过诱导细胞循环骤停度，雷丝晶体显着抑制了IL22诱导的HACAT细胞增殖。此外，IL22显着抑制了HACAT细胞的分化，并且通过雷公酮治疗反转这种现象。相反，雷公藤内酯对IL22刺激的HACAT细胞增殖和分化的影响尤其由miR-181b-5p antagomir逆转。此外，双荧光素酶测定表明，E2F5是HaCAT细胞中miR-181b-5p的直接靶标。同时，MiR-181b-5p的上调明显降低了HaCAT细胞中E2F5的水平。结论：在本研究中，我们发现雷公藤内酯可以通过上调miR-181b-5p来抑制IL22刺激的角质形成细胞中的增殖和促进分化。这些数据表明，雷公藤内酯可以是治疗牛皮癣的潜在剂。

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