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紫草素对再生障碍性贫血小鼠模型中骨髓树突状细胞功能的影响。

Effects of Shikonin on the Functions of Myeloid Dendritic Cells in a Mouse Model of Severe Aplastic Anemia.

机构信息

The Department of Hematology, General Hospital of Tianjin Medical University, Tianjin, China.

出版信息

Mediators Inflamm. 2020 Feb 20;2020:9025705. doi: 10.1155/2020/9025705. eCollection 2020.

DOI:10.1155/2020/9025705
PMID:32148443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7053458/
Abstract

This study is aimed at investigating the effects of shikonin, a pyruvate kinase M2 (PKM2) inhibitor, on the functions of myeloid dendritic cells (mDCs) in a mouse model of severe aplastic anemia (AA) generated by total body irradiation and lymphocyte infusion. Flow cytometry and qPCR were used to determine the proportions of PKM2+ mDCs and other immune indicators in the AA mice. Glucose consumption level, pyruvate generation level, and ATP content were used to determine the level of glycolytic metabolism in the mDCs. The survival rates of AA mice were evaluated after the administration of shikonin or the immunosuppressive agent cyclosporin A. The AA mice displayed pancytopenia, decreased CD4+/CD8+ cell ratio, increased perforin and granzyme levels in CD8+ cells, increased costimulatory CD80 and CD86 expressions, and inadequate regulatory T cell number. animal experiments showed that the shikonin-mediated inhibition of the PKM2 expression in mice was associated with high survival rates. In addition, the administration of cyclosporin A or shikonin decreased the expression of cytotoxic molecules and costimulatory CD80 and CD86 on CD8+ cells. Taken together, the results of this study indicated that shikonin could inhibit the activation and proliferation of mDCs as well as the activation of downstream cytotoxic T cells by reducing the PKM2 level in mDCs.

摘要

本研究旨在探讨吡咯烷酮羧酸（PKM2）抑制剂紫草素对全身辐射和淋巴细胞输注诱导的严重再生障碍性贫血（AA）小鼠模型中髓样树突状细胞（mDC）功能的影响。流式细胞术和 qPCR 用于确定 AA 小鼠中 PKM2+mDCs 和其他免疫指标的比例。葡萄糖消耗水平、丙酮酸生成水平和 ATP 含量用于确定 mDCs 糖酵解代谢水平。在用紫草素或免疫抑制剂环孢素 A 处理后，评估 AA 小鼠的存活率。AA 小鼠表现出全血细胞减少症、CD4+/CD8+细胞比例降低、CD8+细胞中穿孔素和颗粒酶水平升高、共刺激分子 CD80 和 CD86 表达增加以及调节性 T 细胞数量不足。动物实验表明，紫草素介导的 PKM2 表达抑制与高存活率相关。此外，环孢素 A 或紫草素的给药降低了 CD8+细胞上细胞毒性分子和共刺激 CD80 和 CD86 的表达。综上所述，本研究结果表明，紫草素通过降低 mDCs 中的 PKM2 水平，可抑制 mDCs 的激活和增殖以及下游细胞毒性 T 细胞的激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b0/7053458/231a0db957b4/MI2020-9025705.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b0/7053458/6bf0f7ff1875/MI2020-9025705.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b0/7053458/231a0db957b4/MI2020-9025705.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b0/7053458/6bf0f7ff1875/MI2020-9025705.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b0/7053458/f051d2b2fd65/MI2020-9025705.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b0/7053458/7e92999841f4/MI2020-9025705.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7b0/7053458/231a0db957b4/MI2020-9025705.007.jpg

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