中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (3): 404-405.doi: 10.4103/1673-5374.179042

• 观点:退行性病与再生 • 上一篇    下一篇

神经胶质细胞在环己烷致神经变性及再生中的作用

  

  • 收稿日期:2016-02-19 出版日期:2016-03-15 发布日期:2016-03-15
  • 基金资助:

    神经基础和应用心理学研究基金

Glial plasticity after hexahydrobenzene exposure

Tania Campos-Ordonez, Oscar Gonzalez-Perez   

  1. Laboratory of Neurobiology, School of Psychology, University of Colima, Colima, Mexico (Campos-Ordonez T, Gonzalez-Perez O)
    Medical Sciences PhD Program, School of Medicine, University of Colima, Colima, Mexico (Campos-Ordonez T)
  • Received:2016-02-19 Online:2016-03-15 Published:2016-03-15
  • Contact: Oscar Gonzalez-Perez, M.D., Ph.D.,osglez@ucol.mx.
  • Supported by:

    TCO was supported by PhD CONACyT fellowship No. 736339. This work was funded by CONACyT grants No. 268062 and No. 2015-01465.

摘要:

环己烷作为一种有机溶剂普遍存在于一些商业产品如汽油,油漆稀释剂,粘合剂和农药之中。如被滥用的药物,这种物质和其他有机溶剂在全世界大范围内影响着人们的健康。小鼠吸入环己烷刺激反应性胶质细胞增生,小胶质细胞反应以及对大脑产生氧化应激。星形胶质细胞和小胶质细胞在保持局部平衡和维持中枢神经系统结构优化方面发挥着不同的作用。 这些胶质细胞也是抵抗脑损伤的主要因素,但它们在环己烷吸入中的生物学作用尚不清楚。在此,我们总结了关于环己烷对神经组织影响的最先进技术。了解有关环己烷吸入发病机制中的细胞和分子机制是为溶剂使用者设计治疗方法和预防措施的关键一步。

Abstract:

Parkinson disease (PD) is a progressive neurodegenerative disorder clinically characterized by motor symptoms (bradykinesia, tremor, rigidity, postural instability) and non-motor symptoms (hyposmia, sleep disorders, autonomic and sphincteric dysfunctions, fatigue, pain, depression, and cognitive disorders). At the onset of parkinsonian symptoms, the neuron loss is quite 70% in the lateral ventral part and 50% in the caudal part of substantia nigra. For this reason, and for the long time between the cellular onset and the clinical onset of the disease, it is mandatory to develop new therapies with disease-modifying and neuroprotective actions. The gold standard therapy for PD is always levodopa, while other currently validated treatments are dopamine agonists, cathecol-O-methyltransferase inhibitors, monoamine-oxidase-B inhibitors, and amantadine. Recent data showed that in some inherited and degenerative diseases of the nervous system the pathogenesis of the symptoms could be linked to a focal deficiency of thiamine (vitamin B1) due either to dysfunction of intracellular thiamine transport or to structural enzymatic abnormalities. Thiamine is a cofactor of enzymes involved in fundamental pathways of energetic cell metabolism, particularly critical in glucose metabolism. Recent clinical studies showed a considerable and stable improvement of motor and non-motor symptoms in patients affected by PD with intramuscular high-dose thiamine (100 mg) administered twice a week. Therefore, we decided to extend the treatment with high doses of thiamine to a series of PD patients in order to clarify the potential effect of thiamine in this disease. We found that long-term treatment with intramuscular administration of thiamine has led to significant improvement of motor and non-motor symptoms of patients with PD; this improvement was stable during time and without side effects. Our report represents an important contribution to PD therapy, although further experience is necessary to exclude placebo effect and to confirm the present observation, with clinical, cellular, and molecular data. The aim of future studies will be to investigate the clinical, restorative, and neuroprotective effects of long-term treatment with thiamine in PD.