Neural Regeneration Research ›› 2016, Vol. 11 ›› Issue (9): 1438-1444.doi: 10.4103/1673-5374.191217

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Protective effects of carnosine on white matter damage induced by chronic cerebral hypoperfusion

Jing Ma, Shu-hong Bo, Xiao-tong Lu, A-jing Xu*, Jian Zhang*   

  1. Department of Pharmacy, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
  • Received:2016-08-15 Online:2016-09-30 Published:2016-09-30
  • Contact: A-jing Xu, Ph.D. or Jian Zhang, Ph.D., jeta_xu@hotmail.com or zjpharmacy2014@163.com.
  • Supported by:
    This study was funded by the National Natural Science Foundation of China, No. 81402904; the Foundation of Shanghai Jiao Tong University School of Medicine, No. 13XJ22001; the Foundation of Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 13YJ11; a grant from the Science and Technology Commission of Shanghai Municipality of China, No. 13ZR1426900, 15411963900.

Abstract: Carnosine is a dipeptide that scavenges free radicals, inhibits in?ammation in the central nervous system, and protects against ischemic and hypoxic brain damage through its anti-oxidative and anti-apoptotic actions. Therefore, we hypothesized that carnosine would also protect against white matter damage caused by subcortical ischemic injury. White matter damage was induced by right unilateral common carotid artery occlusion in mice. The animals were treated with 200, 500 or 750 mg/kg carnosine by intraperitoneal injection 30 minutes before injury and every other day after injury. Then, 37 days later, Klüver-Barrera staining, toluidine blue staining and immuno?uorescence staining were performed. Carnosine (200, 500 mg/kg) substantially reduced damage to the white matter in the corpus callosum, internal capsule and optic tract, and it rescued expression of myelin basic protein, and alleviated the loss of oligodendrocytes. However, carnosine at the higher dose of 750 mg/kg did not have the same effects as the 200 and 500 mg/kg doses. These fndings show that carnosine, at a particular dose range, protects against white matter damage caused by chronic cerebral ischemia in mice, likely by reducing oligodendroglial cell loss.

Key words: nerve regeneration, subcortical ischemic vascular dementia, carnosine, corpus callosum, neuron, internal capsule, oligodendrocyte, optic tract, white matter damage, neural regeneration