Effect of mild hypothermia on nerve regeneration microenvironment of infarcted area in rat models of cerebral infarction
10.3969/j.issn.2095-4344.2016.27.009
- VernacularTitle:亚低温对构建脑梗死模型大鼠梗死区神经再生微环境的影响
- Author:
Ruijuan ZHENG
;
Yuhong GAO
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2016;20(27):4013-4019
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Numerous studies have demonstrated that mild hypothermia has a better protective effect on neurons after cerebral infarction.
OBJECTIVE:To investigate theeffect of mild hypothermia on nerve regeneration microenvironment of infarcted area in rat models of cerebral infarction and analyze its possible effects on neural functional recovery after cerebral infarction.
METHODS:Twenty out of 65 adult femaleSprague-Dawleyrats were randomly selected as the sham group. The remaining 45 rats were subjected to carotid artery ligation to establish rat models of cerebral infarction. Five rats were rejected because of modeling failureor death, the remaining 40 rats were randomly and evenly divided into cerebralinfarction and mild hypothermia groups. The head temperature of rats in the cerebral infarction group was downregulated to (37±1)℃ using a semiconductor refrigeration instrument. The rats were transferred to the room with the temperature of 25℃ after the operation. Brain hypothermia was also induced in rats from the mild hypothermia group. At 13.0-14.0 minutes after establishing rat models of cerebral ischemia, the head on the side of cerebral ischemia was tightly connected with the probe of the semiconductor refrigeration instrument. The refrigerator temperature was adjusted to 6-8℃, so as to make the temperature of brain tissue on the lesion side at 32.0-33.0℃ for 4 hours.
RESULTS AND CONCLUSION:Compared with the cerebral infarction group, the BBB scores of rats inthe mild hypothermia group were distinctly increased, and the volume of infarcted area decreased. At 1 day after modeling, the expression level of growth associated protein 43 mRNA in brain tissue of rats in the mild hypothermia group was close to that in the cerebral infarction group. At 2 weeks after modeling, the expression level of growthassociated protein 43 mRNAin brain tissue of rats in the mild hypothermia group was significantly increased compared with that in the cerebral infarction group. These results suggest that mild hypothermia therapy can protect nerve cels against injury caused by cerebral infarction and promote the recovery of neurological function. Its underlying mechanism may be related to the up-regulation of the expression of growth associated protein 43 in ischemic penumbra .
