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阻断Tim-3通过抑制神经炎症和促进小胶质细胞从M1型向M2型表型极化来改善脊髓缺血再灌注损伤。

Blocking of Tim-3 Ameliorates Spinal Cord Ischemia-Reperfusion Injury Through Inhibiting Neuroinflammation and Promoting M1-to-M2 Phenotypic Polarization of Microglia.

作者信息

Li Zhenxing, Zhou Binbin, Chen Guanghui, Yang Xiangyu, Su Han, Li Bolin

机构信息

Department of Rehabilitation, First Affiliated Hospital of the Guangxi University of Chinese Medicine, Nanning, Guangxi, China.

Department of Tuina, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi, China.

出版信息

Immun Inflamm Dis. 2024 Dec;12(12):e70084. doi: 10.1002/iid3.70084.

DOI:10.1002/iid3.70084
PMID:39641284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11621861/
Abstract

BACKGROUND

Blocking of Tim-3 exerts therapeutic effects in a series of ischemia-reperfusion injury (IRI).

METHODS

In this work, a cross-clamped aortic arch was conducted to establish SCIRI rat model. Besides, rat spinal microglia was subjected to OGD/R to mimic I/R-like conditions in vitro. The in vivo and in vitro therapeutic effects of Tim-3 antibody in SCIRI were investigated from these aspects: neuronal apoptosis, neuroinflammation, microglia activation, and polarization.

RESULTS

It was verified that Tim-3 was highly expressed in spinal cord tissues of SCIRI rats and blocking of Tim-3 attenuated SCIRI-induced pathological injury, neuronal apoptosis, neuroinflammation, and microglia activation (M1 polarization). In addition, it was verified that Tim-3 was highly expressed in OGD/R-treated rat spinal microglia and blocking of Tim-3 attenuated OGD/R-induced inflammation and spinal microglia activation (M1 polarization).

CONCLUSIONS

Tim-3 antibody can exert therapeutic effects in SCIRI through inhibiting neuroinflammation and promoting microglia polarization from M1 to M2 phenotype.

摘要

背景

阻断Tim-3在一系列缺血再灌注损伤（IRI）中发挥治疗作用。

方法

在本研究中，采用夹闭主动脉弓的方法建立脊髓缺血再灌注损伤（SCIRI）大鼠模型。此外，体外对大鼠脊髓小胶质细胞进行氧糖剥夺/复氧（OGD/R）处理以模拟缺血再灌注样条件。从神经元凋亡、神经炎症、小胶质细胞活化和极化等方面研究Tim-3抗体对SCIRI的体内和体外治疗作用。

结果

证实Tim-3在SCIRI大鼠脊髓组织中高表达，阻断Tim-3可减轻SCIRI诱导的病理损伤、神经元凋亡、神经炎症和小胶质细胞活化（M1极化）。此外，证实Tim-3在OGD/R处理的大鼠脊髓小胶质细胞中高表达，阻断Tim-3可减轻OGD/R诱导的炎症和脊髓小胶质细胞活化（M1极化）。

结论

Tim-3抗体可通过抑制神经炎症和促进小胶质细胞从M1表型向M2表型极化在SCIRI中发挥治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/b1ef0e6ed92d/IID3-12-e70084-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/4c960c013a64/IID3-12-e70084-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/e08d81586224/IID3-12-e70084-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/97723632e8ae/IID3-12-e70084-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/d25020a0932f/IID3-12-e70084-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/06f4ae14a709/IID3-12-e70084-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/60e871999eda/IID3-12-e70084-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abd1/11621861/b1ef0e6ed92d/IID3-12-e70084-g009.jpg

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本文引用的文献

1
The role of TIM-3 in sepsis: a promising target for immunotherapy?TIM-3 在脓毒症中的作用：免疫治疗的有前途靶点？
Front Immunol. 2024 Mar 21;15:1328667. doi: 10.3389/fimmu.2024.1328667. eCollection 2024.
2
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In Vitro Cell Dev Biol Anim. 2024 Mar;60(2):172-182. doi: 10.1007/s11626-023-00846-3. Epub 2024 Jan 16.
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Discovery of TIM-3: Beyond a Th1 Regulator.
TIM-3的发现：超越Th1调节因子
J Immunol. 2024 Feb 1;212(3):359-360. doi: 10.4049/jimmunol.2300682.
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Spinal cord protection for thoracoabdominal aortic aneurysm repair: from bench to bedside.胸腹主动脉瘤修复术中的脊髓保护：从实验台到临床应用
Ann Cardiothorac Surg. 2023 Sep 28;12(5):438-449. doi: 10.21037/acs-2023-scp-08. Epub 2023 May 15.
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T-cell immunoglobulin and mucin-domain containing-3 (TIM-3): Solving a key puzzle in autoimmune diseases.T 细胞免疫球蛋白和黏蛋白结构域蛋白 3（TIM-3）：解决自身免疫性疾病中的关键难题。
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The roles of microRNAs in spinal cord ischemia-reperfusion injury.微小RNA在脊髓缺血再灌注损伤中的作用。
Neural Regen Res. 2022 Dec;17(12):2593-2599. doi: 10.4103/1673-5374.339471.
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Distinct Polarization Dynamics of Microglia and Infiltrating Macrophages: A Novel Mechanism of Spinal Cord Ischemia/Reperfusion Injury.小胶质细胞和浸润性巨噬细胞独特的极化动力学：脊髓缺血/再灌注损伤的新机制
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