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双氢青蒿素通过抑制转录因子 SNAI1 来保护脓毒症期间的血脑屏障通透性。

Dihydroartemisinin protects blood-brain barrier permeability during sepsis by inhibiting the transcription factor SNAI1.

机构信息

School of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.

Medical Research Center, the First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China.

出版信息

Clin Exp Pharmacol Physiol. 2022 Sep;49(9):979-987. doi: 10.1111/1440-1681.13683. Epub 2022 Jun 24.

DOI:10.1111/1440-1681.13683
PMID:35651290
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9543489/
Abstract

Blood-brain barrier (BBB) injury is involved in the pathogenesis of sepsis-associated encephalopathy. In this study, we used dihydroartemisinin (DHA), a derivative of artemisinin, to treat a cecal ligation and puncture (CLP)-induced mouse sepsis model and a tumour necrosis factor α (TNF-α)-stimulated human cerebral microvessel endothelial cells (hCMEC)/D3 cell line. We found that DHA decreased BBB permeability and increased the expression of the tight junction protein occludin (OCLN) in the CLP model. In hCMEC/D3 cells, DHA decreased TNF-α-induced hyperpermeability and increased the expression of OCLN. DHA also repressed SNAI1 expression in the CLP mouse model and in TNF-α-stimulated hCMEC/D3 cells. These data suggest that DHA protects BBB permeability during sepsis by stimulating the expression of OCLN, by downregulating the expression of the SNAI1 transcription factor.

摘要

血脑屏障（BBB）损伤与脓毒症相关性脑病的发病机制有关。在本研究中，我们使用青蒿素衍生物二氢青蒿素（DHA）治疗盲肠结扎和穿刺（CLP）诱导的小鼠脓毒症模型和肿瘤坏死因子α（TNF-α）刺激的人脑血管内皮细胞（hCMEC）/D3 细胞系。我们发现 DHA 降低了 BBB 的通透性，并增加了 CLP 模型中紧密连接蛋白 occludin（OCLN）的表达。在 hCMEC/D3 细胞中，DHA 降低了 TNF-α诱导的高通透性，并增加了 OCLN 的表达。DHA 还抑制了 CLP 小鼠模型和 TNF-α刺激的 hCMEC/D3 细胞中 SNAI1 的表达。这些数据表明，DHA 通过刺激 OCLN 的表达，下调 SNAI1 转录因子的表达，在脓毒症期间保护 BBB 的通透性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/8dd9e5382c07/CEP-49-979-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/e42ccc737759/CEP-49-979-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/4a445ce033a6/CEP-49-979-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/64d71e6b520a/CEP-49-979-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/b2c103dadf38/CEP-49-979-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/8dd9e5382c07/CEP-49-979-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/e42ccc737759/CEP-49-979-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/4a445ce033a6/CEP-49-979-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/64d71e6b520a/CEP-49-979-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/b2c103dadf38/CEP-49-979-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0369/9543489/8dd9e5382c07/CEP-49-979-g003.jpg

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