Spinal cord injury and its underlying mechanism in rats with temporal lobe epilepsy

Liu,Jinjie; Liu,Zanhua; Liu,Guoliang; Gao,Kai; Zhou,Hengjie; Zhao,Yongbo; Wang,Hong; Zhang,Lin; Liu,Sibo

doi:10.3892/etm.2020.8453

March-2020 Volume 19 Issue 3

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March-2020 Volume 19 Issue 3

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Article Open Access

Spinal cord injury and its underlying mechanism in rats with temporal lobe epilepsy

Authors:
- Jinjie Liu
- Zanhua Liu
- Guoliang Liu
- Kai Gao
- Hengjie Zhou
- Yongbo Zhao
- Hong Wang
- Lin Zhang
- Sibo Liu
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Affiliations: General Ward II, Affiliated Municipal Central Hospital of Dalian Medical University, Dalian, Liaoning 116000, P.R. China, Department of Neurology, Nanjing Gaochun People's Hospital, Gaochun, Nanjing 210000, P.R. China, Surgical Intensive Care Unit, Dalian Municipal Central Hospital, Dalian, Liaoning 116000, P.R. China, Department of Neurology, The First People's Hospital of Shanghai Jiaotong University, Shanghai 200000, P.R. China, Department of Neurology, Affiliated Municipal Central Hospital of Dalian Medical University, Dalian, Liaoning 116000, P.R. China

Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 2103-2112
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Published online on: January 15, 2020

https://doi.org/10.3892/etm.2020.8453
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Abstract

Numerous cases of spinal cord injury following seizure have been previously reported. However, whether spinal cord injury is a common occurrence after seizures and its underlying mechanisms remain unclear. The present study generated a Sprague‑Dawley rat model of temporal lobe epilepsy (TLE), and Nissl staining and transmission electron microscopy were used to detect tissue damage. In addition, Evans blue staining was used to detect damage to the blood‑brain barrier (BBB) and albumin extravasation. In addition, double‑staining was used to detect the association between neurons and extravasated albumin. Furthermore, neuronal degeneration was assessed using Fluoro‑Jade C staining, while fluorescence staining and western blotting were used to detect apoptosis and inflammation. In the present study, spinal cord injury was only observed in rats with grade IV‑V seizures, whereas Nissl staining showed structural damage and decreased neuronal cell numbers in the brain and the spinal cord. The present study identified BBB damage and albumin extravasation in rats of the TLE groups. Double‑staining for albumin and neurons showed a significant match of neurons positive for albumin. Fluoro‑Jade C staining indicated neuronal degeneration in the brain, but not the spinal cord in the TLE rats. High levels of caspase‑3 were also detected in the injured spinal cord. A small number of albumin+ neurons in the spinal cord presented caspase‑3+ signals in rats of the TLE groups. The expression levels of intercellular adhesion molecule 1, CD11b and inflammatory factors such as tumor necrosis factor‑α and interleukin‑6 were significantly elevated in the injured spinal cord. The present results suggested that spinal cord injury occurred in rats as a result of severe seizure attacks, and that BBB damage, albumin extravasation, inflammation and apoptosis contributed to the pathological changes observed during spinal cord injury.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Spinal cord injury and its underlying mechanism in rats with temporal lobe epilepsy

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