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

Immunity, Inflammation and Disease, 2024 · DOI: https://doi.org/10.1002/iid3.70084 · Published: November 13, 2024

Spinal Cord Injury Cardiovascular Science Immunology

Simple Explanation

Spinal cord ischemia-reperfusion injury (SCIRI) can lead to irreversible damage. Currently, there is a lack of effective strategies to ameliorate SCIRI. This research investigates the role of Tim-3 in SCIRI. The study uses a SCIRI rat model and OGD/R-treated rat spinal microglia to investigate the therapeutic effects of a Tim-3 antibody. The investigation focuses on neuronal apoptosis, neuroinflammation, microglia activation, and polarization. The results suggest that Tim-3 antibody can exert therapeutic effects in SCIRI. This is achieved by inhibiting neuroinflammation and promoting microglia polarization from the M1 to M2 phenotype.

Study Duration

Not specified

Participants

SD rats (200–250 g), 16 SCI patients, and 6 volunteers

Evidence Level

Not specified

Key Findings

1
Tim-3 is highly expressed in spinal cord tissues of SCIRI rats. Blocking Tim-3 attenuated SCIRI-induced pathological injury, neuronal apoptosis, neuroinflammation, and microglia activation (M1 polarization).
2
Tim-3 was highly expressed in OGD/R-treated rat spinal microglia. Blocking Tim-3 attenuated OGD/R-induced inflammation and spinal microglia activation (M1 polarization).
3
Tim-3 antibody can exert therapeutic effects in SCIRI. It achieves this through inhibiting neuroinflammation and promoting microglia polarization from M1 to M2 phenotype.

Research Summary

This study investigates the role of Tim-3 in spinal cord ischemia-reperfusion injury (SCIRI) using a rat model and in vitro experiments. The aim is to explore potential therapeutic effects of a Tim-3 antibody. The research found that Tim-3 is highly expressed in SCI patients and spinal cord tissues of SCIRI rats. Blocking Tim-3 mitigates pathological injury and neuronal apoptosis after SCIRI. The study concludes that Tim-3 antibody can exert therapeutic effects in SCIRI by inhibiting neuroinflammation and promoting microglia polarization from M1 to M2 phenotype.

Practical Implications

Therapeutic Potential

Tim-3 antibody shows promise as a therapeutic agent for SCIRI by reducing neuroinflammation and promoting microglia polarization.

Microglia Polarization

Promoting microglia polarization from M1 to M2 phenotype could be a key strategy in ameliorating SCIRI.

Biomarker Identification

Tim-3 expression levels could potentially serve as a biomarker for the severity and progression of SCIRI.

Study Limitations

1
The study relies on animal models and in vitro experiments. Further research is needed to confirm the findings in human clinical trials.
2
Further research is needed to analyze the association between Tim-3 expression and clinical features of SCIRI.
3
Application of transgenic animals is needed to further verify the therapeutic effects of Tim‐3 antibody in SCIRI.

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