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.
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.
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。
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