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  1. Mayaki AM, Abdul Razak IS, Mohd Adzahan N, Mazlan M, Abdullah R
    J Equine Vet Sci, 2020 07;90:103019.
    PMID: 32534783 DOI: 10.1016/j.jevs.2020.103019
    Equine chronic back pain (CBP) has been linked to different pathologic processes, which directly or indirectly involve spinal structures. Thus, making diagnosis and management very challenging with most horses with the condition recommended for early retirement from athletic activity. This study described the spinal cord lesions and the development of reactive microgliosis and astrocytosis in the spinal cords of horse with CBP. Thoracolumbar spinal cord segments from three horses euthanized because of unresolved CBP were dissected and grossly and histopathologically examined. The expression of activated microglia and astrocytes were demonstrated immunohistochemically using polyclonal rabbit anti-Iba-1 and anti-glial fibrillary acidic protein antibodies, respectively. All horses had radiological evidence of varying degrees of kissing spine involving six to nine vertebrae with the majority of the lesions graded between 2 and 5. Grossly, there was myelomalacia with intramedullary hemorrhages. The gray matters of the spinal cords were characterized by hemorrhagic malacic lesions with medullary disintegration. Reactive microgliosis and astrocytosis were evident in the spinal dorsal horns. White matter lesions include axonal swollen and/or loss, satellitosis, and varying degrees of dilation of myelin sheaths with some containing macrophages. In conclusion, the presence of reactive microgliosis and astrogliosis in the spinal dorsal horn indicates that they are possible precipitating factors in the development of equine CBP.
    Matched MeSH terms: Gliosis/veterinary
  2. Suryaningtyas W, Parenrengi MA, Bajamal AH, Rantam FA
    Malays J Med Sci, 2020 May;27(3):34-42.
    PMID: 32684804 DOI: 10.21315/mjms2020.27.3.4
    Background: Hydrocephalus induces mechanical and biochemical changes in neural cells of the brain. Astrogliosis, as the hallmark of cellular changes in white matter, is involved in demyelination process, re-myelination inhibitory effect, and inhibition of axonal elongation and regeneration. The pathophysiology of this process is not well understood. The purpose of the present study is to elucidate the effect of lipid peroxidation product on astrogliosis through WNT/ β-catenin in kaolin-induced hydrocephalic rats.

    Methods: The study used kaolin-induced hydrocephalic rats. Obstructive hydrocephalus was expected to develop within seven days after induction. The hydrocephalus animals were killed at day 7, 14 and 21 after induction. One group of the saline-injected animals was used for sham-treatment.

    Results: We demonstrated that the hydrocephalic rats exhibited a high expression of 4-hydroxynonenal (4-HNE) in the periventricular area. The expression of β-catenin also increased, following the pattern of 4-HNE. Reactive astrocyte, expressed by positive glial fibrillary acidic protein (GFAP), was upregulated in an incremental fashion as well as the microglia.

    Conclusion: This work suggests that lipid peroxidation product, 4-HNE, activated the WNT/β-catenin pathway, leading to the development of reactive astrocyte and microglia activation in hydrocephalus.

    Matched MeSH terms: Gliosis
  3. Dahmardeh N, Shabani M, Basiri M, Kalantaripour TP, Asadi-Shekaari M
    Malays J Med Sci, 2019 Jul;26(4):28-38.
    PMID: 31496891 DOI: 10.21315/mjms2019.26.4.4
    Background: There is a meaningful necessity for a targeted therapy of essential tremor (ET), as medications have not been developed specifically for ET. For nearly a century, many drugs have been applied in the treatment of tremor but the drug treatment of ET remains still unknown. Some potential therapeutic factors such fingolimod (FTY720) can be effectively used to treat ET in animals. In the present research, the effect of FTY720, the immunomodulatory sphingosine 1-phosphate (S1P) analog, on degeneration of cerebellar and olivary neurons induced by harmaline in male rats was investigated.

    Methods: The animals were allotted into control dimethyl sulfoxide (DMSO), saline + harmaline [30 mg/kg, intraperitoneally, (i.p.)], harmaline + FTY720 (1 mg/kg, i.p, 1 h and 24 h before harmaline injection) groups (n = 10). The cerebellum and inferior olive nucleus (ION) were studied for neuronal degeneration using immunohistochemistry (IHC) and ultrastructural study by transmission electron microscopy (TEM) techniques.

    Results: Harmaline caused neuronal cell loss, caspase-3 mediated apoptosis, astrocytosis and ultrastructural changes in cerebellar Purkinje cells and inferior olive neurons. FTY720 exhibited neuroprotective effects on cerebellar Purkinje cells and inferior olivary neurons.

    Conclusion: These results suggest that FTY720 has potential efficacy for prevention of ET neurodegeneration and astrocytosis induced by harmaline in male rats.

    Matched MeSH terms: Gliosis
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