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氯原酸处理对深低温停循环后神经炎症的有益作用可能是通过 CYLD/NF-κB 信号传导介导的。

Beneficial effects of chlorogenic acid treatment on neuroinflammation after deep hypothermic circulatory arrest may be mediated through CYLD/NF-κB signaling.

机构信息

Department of Cardiac Surgery, Fujian Branch of Shanghai Children's Medical Cente, Fuzhou, China; Fujian Children's Hospital, Fuzhou, China; Fujian Maternity and Child Health Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, China; Fujian Key Laboratory of Women and Children's Critical Diseases Research, Fujian Maternity and Child Health Hospital, Fuzhou, China.

Department of Cardiac Surgery, Fujian Branch of Shanghai Children's Medical Cente, Fuzhou, China; Fujian Children's Hospital, Fuzhou, China; Fujian Maternity and Child Health Hospital, Affiliated Hospital of Fujian Medical University, Fuzhou, China; Fujian Key Laboratory of Women and Children's Critical Diseases Research, Fujian Maternity and Child Health Hospital, Fuzhou, China.

出版信息

Brain Res. 2021 Sep 15;1767:147572. doi: 10.1016/j.brainres.2021.147572. Epub 2021 Jun 30.

DOI:10.1016/j.brainres.2021.147572
PMID:34216581
Abstract

Deep hypothermic circulatory arrest (DHCA) during heart surgery may induce neuroinflammation leading to neurocognitive dysfunction. Chlorogenic acid (CA) is a common phytochemical, which can attenuate neuroinflammation. Nevertheless, the underlying mechanism involved in the anti-inflammatory effect of CA after DHCA is unknown. The present study therefore characterized the anti-inflammatory functions of CA after DHCA using in vivo and in vitro DHCA models. The activation of microglia, inflammatory cytokine levels, and the NF-κB pathway were measured. The results showed that CA treatment ameliorated neurocognitive function and reduced the inflammatory cytokine levels in the brain and circulation. Furthermore, the microglial and NF-κB activations were suppressed after DHCA. CA exerted the same anti-inflammatory effect in hypothermia OGD microglial cells as the in vivo study. Additional studies indicated that the regulation of ubiquitin ligase activity of TRAF6 and RIP1 by CYLD was related to the mechanism involving inhibition of CA in the NF-κB pathway. Together, the results showed that CA may attenuate neuroinflammation after DHCA by modulating the signaling of CYLD/NF-κB.

摘要

深低温停循环(DHCA)期间的心脏手术可能会引发神经炎症,导致神经认知功能障碍。绿原酸(CA)是一种常见的植物化学物质,可减轻神经炎症。然而,CA 在 DHCA 后抗炎作用的潜在机制尚不清楚。因此,本研究使用体内和体外 DHCA 模型来描述 CA 在 DHCA 后的抗炎功能。测量了小胶质细胞的激活、炎性细胞因子水平和 NF-κB 途径。结果表明,CA 治疗可改善神经认知功能并降低大脑和循环中的炎症细胞因子水平。此外,DHCA 后小胶质细胞和 NF-κB 的激活受到抑制。CA 在低温 OGD 小胶质细胞中的抗炎作用与体内研究相同。进一步的研究表明,CYLD 对 TRAF6 和 RIP1 的泛素连接酶活性的调节与 CA 抑制 NF-κB 途径的机制有关。总之,研究结果表明 CA 可能通过调节 CYLD/NF-κB 信号通路来减轻 DHCA 后的神经炎症。

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