DHA plays a protective role in cerebral ischemia–reperfusion injury by affecting macrophage/microglia type polarization

IF 2.7 4区医学 Q3 NEUROSCIENCES

Brain Research Pub Date : 2024-10-14 DOI:10.1016/j.brainres.2024.149278

Jin Yimin , Pu Tiantian , Zhang Tongshuai , Sun Qixu , Han Yang , Han Siyu , Wang Guangyou , Yang Shanshan , Zhang Yao

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引用次数: 0

Abstract

A close correlation exists between the macrophage/microglia(MΦ/MG) polarization states and the development of cerebral ischemia and reperfusion (I/R). Therefore it is of great significance to research on how to modulate the MΦ/MG states for improved patient outcomes. In particular, regulatory mechanisms involved in this process remain to be identified. Hereby, we aim to shed light on how docosahexaenoic acid (DHA) actively modulates the switch between M1 and M2 macrophage states by restraining the NACHT-LRR-PYD-containing protein three inflammasome (NALP3). We found that NALP3-positive cells were detected in clinical human cerebral infarction tissue samples and the mouse tMCAO model. In mice after DHA treatment, the number of NALP3-positive cells was significantly reduced, significantly decreasing infarct volume and improving the postoperative physical status of mice. NALP3-positive cells were found to be MΦ/MG after co-staining with CD11b. By extracting peritoneal macrophages, it was verified that DHA inhibited the activation of NALP3 and regulated the transformation of M1 and M2 cells, thereby reducing I/R injury.

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DHA 通过影响巨噬细胞/小胶质细胞的极化类型，在脑缺血再灌注损伤中发挥保护作用。

巨噬细胞/小胶质细胞（MΦ/MG）的极化状态与脑缺血和再灌注（I/R）的发生密切相关。因此，研究如何调节 MΦ/MG 状态以改善患者预后具有重要意义。特别是，参与这一过程的调控机制仍有待确定。在此，我们旨在揭示二十二碳六烯酸（DHA）如何通过抑制含NACHT-LRR-PYD蛋白的三炎症小体（NALP3）来积极调节M1和M2巨噬细胞状态之间的转换。我们发现，在临床人类脑梗塞组织样本和小鼠 tMCAO 模型中都检测到了 NALP3 阳性细胞。小鼠经 DHA 治疗后，NALP3 阳性细胞的数量明显减少，梗死体积明显缩小，术后身体状况明显改善。NALP3阳性细胞与CD11b共染后发现是MΦ/MG。通过提取腹腔巨噬细胞，验证了 DHA 可抑制 NALP3 的活化，调节 M1 和 M2 细胞的转化，从而减轻 I/R 损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Brain Research 医学-神经科学

CiteScore

5.90

自引率

3.40%

发文量

268

审稿时长

47 days

期刊介绍： An international multidisciplinary journal devoted to fundamental research in the brain sciences. Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed. With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.