Spinal cord injury (SCI) is a serious and complex medical condition that can happen to anyone. At present, therapy mainly focuses on rehabilitation and pharmacological treatment, such as methylprednisolone (MP). Supra-spinal changes in certain structures, such as the cerebellum, that receive many afferents from the spinal cord might be one reason for unsuccessful therapeutic outcomes. Recently, the expression of FNDC5 was reported in cerebellar Purkinje cells as a possible neuroprotective agent. In the present study, we considered the expression of FNDC5 in Purkinje cells following SCI with and without MP administration in adult rats with SCI. Thirty-five adult male rats were used in this study. The animals were randomly allocated into five groups, including SCI, spinal cord injury with methylprednisolone treatment (SCI + MP), operation sham, control, and operation sham with MP. Induction of SCI was achieved by using special clips to compress the spinal cord at a determined level. After a certain interval time, the animals underwent study for FNDC5 expression, apoptosis by using immunohistochemistry, Western blotting, and TUNEL and Nissl staining. Our results showed a significant decrease in the number of Purkinje cells following SCI. Therapy with MP inhibits apoptosis in irFNDC5 Purkinje cells and restores them. Expression of FNDC5 significantly increased in SCI and decreased following MP therapy. We also showed other cerebellar cells with FNDC5 immunoreactivity in the two other cerebellar layers that were firstly reported. Since irisin is known as a plasma product of FNDC5, we think it might be a plasma marker following therapeutic efforts for SCI; however, it needs further research. In addition, it is possible that changes in FNDC5 expression in Purkinje cells might be related to neurogenesis in the cerebellum with unknown mechanisms.
Keywords: FNDC5; Irisin; Methylprednisolone; Purkinje cells; Spinal cord injury.
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