Chinese Journal of Tissue Engineering Research ›› 2010, Vol. 14 ›› Issue (45): 8403-8406.doi: 10.3969/j.issn.1673-8225.2010.45.011

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Ischemic tolerance in the brain and proliferation of autologous neural stem cells in rats

Jiang Xiao-feng1, Luo Zu-ming2   

  1. 1 Department of Neurology, Henan People’s Hospital, Zhengzhou  450003, Henan Province, China; 2 West China Hospital, Sichuan University, Chengdu  610041, Sichuan Province, China
  • Online:2010-11-05 Published:2010-11-05
  • Contact: Luo Zu-ming, Master, Professor, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
  • About author:Jiang Xiao-feng☆, Doctor, Attending physician, Department of Neurology, Henan People’s Hospital, Zhengzhou 450003, Henan Province, China simonyes@163.com

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Abstract:

BACKGROUND: Brain ischemic tolerance and autologous neural stem cells have protective effects on the brain, but whether the former can contribute to the proliferation of autologous neural stem cells remains unclear.
OBJECTIVE: To explore the relationship between ischemic preconditioning in brain and proliferation of endogenous neural stem cells in the hippocampus at 7 days following cerebral infarction, and to observe influence of ischemic preconditioning on the status of rats’ neurological deficit after cerebral infarction.
METHODS: The focal-focal ischemic tolerance models of Sprague Dawley rats were established using the twice suture method. A total of 40 male Sprague Dawley rats were randomly divided into sham surgery group, ischemia group, sham surgery + ischemia group and ischemic preconditioning + ischemia group, with 10 rats in each group. The neurological status was assessed using Zea-Longa neurological deficit scores at 3 and 7 days following cerebral infarction. Fluorescent immunohistochemistry was utilized to determine the number of BrdU-positive cells in the hippocampus of the ischemic side of rats.
RESULTS AND CONCLUSION: Zea-Longa neurological deficit scores were lower in the ischemic preconditioning + ischemia group compared with ischemia group and sham surgery + ischemia group at 3 and 7 days following cerebral infarction (P < 0.01). There was no significant difference between ischemia group and sham surgery + ischemia group (P > 0.05). At 7 days following cerebral infarction, the number of BrdU-positive cells in the hippocampus of ischemic side was greater in the ischemia group, sham surgery + ischemia group and ischemic preconditioning + ischemia group compared with sham surgery group (P < 0.01); the number was greater in the ischemic preconditioning + ischemia group compared with ischemia group and sham surgery+ ischemia group (P < 0.01). No significant difference was determined between ischemia group and sham surgery + ischemia group (P > 0.05). Results suggest that ischemic preconditioning could facilitate the proliferation of endogenous neural stem cells in hippocampus dentate gyrus infragranular layer after ischemic cerebral infarction in rats, and improve the status of rats’ neurological deficits.

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