Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (19): 1753-1762.doi: 10.4103/1673-5374.143419

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Inflammatory response and neuronal necrosis in rats with cerebral ischemia

Lingfeng Wu 1, 2, Kunnan Zhang 1, Guozhu Hu 3, Haiyu Yang 3, Chen Xie 3, Xiaomu Wu 1   

  1. 1 Nanchang University Medical College, Nanchang, Jiangxi Province, China
    2 Department of Neurology, People’s Hospital of Jiangxi Province, Nanchang, Jiangxi Province, China
    3 Institution of Neurology, People’s Hospital of Jiangxi Province, Nanchang, Jiangxi Province, China
  • Received:2014-06-25 Online:2014-10-15 Published:2014-10-15
  • Contact: Xiaomu Wu, M.D., Nanchang University Medical College, Nanchang 330006, Jiangxi Province, China, wu0709@hotmail.com.
  • Supported by:

    This project was supported by the National Natural Science Foundation of China, No. 81160148; the Natural Science Foundation of Jiangxi Province, No. 2011033.

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Abstract:

In the middle cerebral artery occlusion model of ischemic injury, inflammation primarily occurs in the infarct and peripheral zones. In the ischemic zone, neurons undergo necrosis and apoptosis, and a large number of reactive microglia are present. In the present study, we investigated the pathological changes in a rat model of middle cerebral artery occlusion. Neuronal necrosis appeared 12 hours after middle cerebral artery occlusion, and the peak of neuronal apoptosis appeared 4 to 6 days after middle cerebral artery occlusion. Inflammatory cytokines and microglia play a role in damage and repair after middle cerebral artery occlusion. Serum intercellular cell adhesion molecule-1 levels were positively correlated with the permeability of the blood-brain barrier. These findings indicate that intercellular cell adhesion molecule-1 may be involved in blood-brain barrier injury, microglial activation, and neuronal apoptosis. Inhibiting blood-brain barrier leakage may alleviate neuronal injury following ischemia.

Key words: nerve regeneration, middle cerebral artery occlusion, inflammatory reactions, intercellular cell adhesion molecule-1, neurons, blood-brain barrier, microglia, NSFC grant, neural regeneration