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Article

Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells

  • Authors:
    • Ying Wang
    • Li Guo
    • Jueqiong Wang
    • Wei Shi
    • Zhilun Xia
    • Bin Li
  • View Affiliations / Copyright

    Affiliations: Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China
  • Pages: 4113-4119
    |
    Published online on: September 13, 2019
       https://doi.org/10.3892/etm.2019.8005
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Abstract

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system characterized by neuronal demyelination. MS pathogenesis occurs via multiple mechanisms, and is mediated in part by oligodendrocyte apoptosis and a robust inflammatory response. In the present study, Necrostatin‑1 (Nec‑1), a specific inhibitor of the receptor‑interacting protein 1 kinase domain, was revealed to effectively alleviate the severity and pathological damage associated with experimental autoimmune encephalomyelitis (EAE), a commonly used mouse model of MS. In addition, treatment with Nec‑1 significantly decreased the number of lesions and inflammatory cell infiltrates in spinal cord tissues, as well as the production of associated pro‑inflammatory cytokines, including tumor necrosis factor α (TNFα), interferon‑γ and interleukin‑1β. Nec‑1 also suppressed TNFα + zVAD‑fmk‑induced apoptosis and necroptosis in primary oligodendrocyte precursor cells. The present study revealed that Nec‑1 effectively attenuated the progression of EAE by suppressing apoptosis and necroptosis in oligodendrocytes, and represents a potential novel therapeutic agent for the treatment of MS.
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Copy and paste a formatted citation
Spandidos Publications style
Wang Y, Guo L, Wang J, Shi W, Xia Z and Li B: Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells. Exp Ther Med 18: 4113-4119, 2019.
APA
Wang, Y., Guo, L., Wang, J., Shi, W., Xia, Z., & Li, B. (2019). Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells. Experimental and Therapeutic Medicine, 18, 4113-4119. https://doi.org/10.3892/etm.2019.8005
MLA
Wang, Y., Guo, L., Wang, J., Shi, W., Xia, Z., Li, B."Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells". Experimental and Therapeutic Medicine 18.5 (2019): 4113-4119.
Chicago
Wang, Y., Guo, L., Wang, J., Shi, W., Xia, Z., Li, B."Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells". Experimental and Therapeutic Medicine 18, no. 5 (2019): 4113-4119. https://doi.org/10.3892/etm.2019.8005
Copy and paste a formatted citation
x
Spandidos Publications style
Wang Y, Guo L, Wang J, Shi W, Xia Z and Li B: Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells. Exp Ther Med 18: 4113-4119, 2019.
APA
Wang, Y., Guo, L., Wang, J., Shi, W., Xia, Z., & Li, B. (2019). Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells. Experimental and Therapeutic Medicine, 18, 4113-4119. https://doi.org/10.3892/etm.2019.8005
MLA
Wang, Y., Guo, L., Wang, J., Shi, W., Xia, Z., Li, B."Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells". Experimental and Therapeutic Medicine 18.5 (2019): 4113-4119.
Chicago
Wang, Y., Guo, L., Wang, J., Shi, W., Xia, Z., Li, B."Necrostatin‑1 ameliorates the pathogenesis of experimental autoimmune encephalomyelitis by suppressing apoptosis and necroptosis of oligodendrocyte precursor cells". Experimental and Therapeutic Medicine 18, no. 5 (2019): 4113-4119. https://doi.org/10.3892/etm.2019.8005
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