中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (1): 92-93.doi: 10.4103/1673-5374.175051

• 观点:脊髓损伤修复保护与再生 • 上一篇    下一篇

半乳糖凝集素-3缺失可减轻神经炎症改善损伤脊髓功能恢复

  

  • 收稿日期:2015-12-18 出版日期:2016-01-15 发布日期:2016-01-15

Absence of galectin-3 attenuates neuroinflammation improving functional recovery after spinal cord injury

Caio Andrade Prins, Fernanda Martins Almeida, Ana Maria Blanco Martinez   

  1. Laboratório de Neurodegeneração e Reparo - Departamento de Patologia -Faculdade de Medicina – HUCFF –UFRJ – Rio de Janeiro – RJ, Brazil (Prins CA, Almeida FM, Martinez AMB)
    Instituto de Ciência Biomédicas, UFRJ, Rio de Janeiro, RJ, Brazil (Almeida FM)
  • Received:2015-12-18 Online:2016-01-15 Published:2016-01-15
  • Contact: Ana Maria Blanco Martinez, M.D., Ph.D.,martinez@histo.ufrj.br.

摘要:

galetin-3缺失情况下脊髓损伤小鼠运动功能能够更好的恢复。半乳糖凝集素3对诱发炎症,妨碍神经再生和减少功能恢复的M1和M2有作用。因此,抑制半乳糖凝集素3治疗可能会提高脊髓损伤治疗效果,从而提高脊髓损伤患者生活质量。文章对半乳凝素-3对神经再生和神经炎症反应的作用,如神经变性疾病和外伤性损伤到神经系统,以及适应性免疫系统中间体如何在确定细胞反应之间的边界的研究进行了综述。

Abstract:

After spinal cord injury, a cascade of events begins. At first, there is physical damage with disruption of the blood brain barrier (BBB) and the integrity of the nervous tissue. The disruption of central nervous system BBB alters the endothelial permeability, the protein and chemokines expression and the propensity to in situ release of inflammatory cytokines overcoming anti-inflammatory signals, facilitating the attraction and entry of immune system cells into the injured spinal cord parenchyma. As a result there is a neuroinflammatory response with changes in blood flow, edema, cell infiltration, apoptosis and release of axonal growth inhibitory factors. Nerve function loss occurs when the nerve impulse propagation is interrupted and do not reach its target. This disorder encompasses neuron and glia apoptosis, accompanied by Wallerian Degeneration of disconnected axons, and central nervous system cells exposure to a hostile microenvironment that hampers axon regeneration. Additionally, the damage spreads further in a phenomenon called progressive hemorrhagic necrosis – PHN, with the appearance of petechial hemorrhagic foci and deterioration in areas outside the lesion epicenter during the next 2 – 24 hours after the trauma. Our laboratory investigates the role of galectin-3, a protein linked to mechanisms of inflammation, behind the cellular mechanisms of neural degeneration/regeneration with perspectives of a novel treatment.