Protective effect of sub-hypothermia on brain tissues of rats after cerebral ischemia reperfusion
- VernacularTitle:亚低温对大鼠缺血再灌注脑组织的保护作用
- Author:
Fang LING
;
Xinguo YE
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2006;10(24):175-177
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: At present, more and more people pay attention to the protection of sub-hypothermia on cerebral ischemic tissue and the effect of sub-hypothermia treatment on inflammatory reaction after cerebral ischemia-reperfusion.OBJECTIVE: To investigate the effect of sub-hypothermia on inflammatory cytokine in cerebral ischemic area of rats and protection on cerebral reperfusion injury.DESIGN: Randomized controlled study on the basis of animals.SETTLNG: People's Hospital of Hubei Province.MATERIALS: The experiment was completed at Laboratory Center of Renmin Hospital of Wuhan University from October 2004 to February 2005. Totally 50 healthy SD rats of clean grade were selected in this study.METHODS: Ten SD rats were divided randomly into normal group and sham operation group with 5 in each group. Other 40 rats were divided randomly into normal temperature cerebral ischemia group and sub-hypothermia cerebral ischemia group with 20 in each group. Rats except 5 in normal group were used to establish reversible ligation model of left middle cerebral artery (MCA) with Longa ligation method. Rats in sham operation group and normal temperature group were put in 20 ℃ room, and anus temperature was maintained at 37 ℃; rats in sub-hypothermia group were put in 4 ℃ room and anus temperature was maintained at (33.0±1.0) ℃.Rats in sub-hypothermia group were treated with sub-hypothermia on whole body, after ischemia, temperature was changed normally, and reperfusion was started 3 hours after cerebral ischemia. All modeling rats were scored with neurological defect: 0 point: none of neurological defect; 1 point: unable to unfold bilateral anterior claws; 2 points: cycling to hemiplegia side during walking; 3 points: falling to hemiplegia side; 4 points: unable to self-walk and with unconsciousness.MAIN OUTCOME MEASURES: Expression of tumor necrosis factor (TNF) andinterleukin-1 in cerebral tissue of ischemic rats, percentage of volume of cerebral infarction,and neurological functional scores.RESULTS: Fifteen rats were excluded because of intracranial hemorrhage,anesthetic accident and unqualified neurological functional scores. Other 15 rats with successful modeling were supplied randomly, and totally 50rats entered the final analysis. ① Number of TNF positive cell in immunohistochemical staining: There were no significant differences between normal group and sham operation group [(3.54±1.24, 3.71±1.50) /sight]; but numbers in sub-hypothermia group were lower than those in normal temperature group [(31.94±7.23, 69.20±9.43)/sight, F=179.16, P ＜ 0.001]. ②Numbers of interleukin-1 positive cells in immunohistochemical staining:There were not significant differences between normal group and sham operation group [(3.20±1.34, 3.89±2.08) /sight]; but numbers in sub-hypothermia group were lower than those in normal temperature group [(28.95±4.97, 55.79±7.93)/sight, F=174.95, P ＜ 0.001]. ③ Volume percentage of infarct focus: Percentage in sub-hypothermia group was lower than that in normal temperature group [(21.06±2.42)%, 30.32±2.71], F =374.87, P ＜ 0.001]. ④ Neurological functional scores: Percentage in subhypothermia group was lower than that in normal temperature group [(1.35±0.27)%, (2.04±0.34)%, F=117.17, P ＜ 0.001].CONCLUSION: ① Volume of cerebral infarction focus is lower in subhypothermia group than that in normal temperature group, this suggests that sub-hypothermia can protect ischemic neurons. ② Positive expressions of TNF and interleukin-1 are observed rarely in normal group and sham operation group, but more expression of positive cells are observed in cerebral ischemic area with 24-hour reperfusion after ischemia, this suggests that cerebral ischemia starts expression of inflammatory cytokine, evoke inflammatory cascade reaction, deteriorate cerebral ischemia-reperfusion injury. Therefore, inhibition of inflammatory cascade reaction is one of important mechanisms of protecting brain.
