| 洪焕茂 谢秋幼 倪啸晓 周锋 虞容豪.高压氧预处理对大鼠局灶性脑缺血再灌注损伤的保护作用[J].现代生物医学进展英文版,2015,15(20):3830-3834. |
| 高压氧预处理对大鼠局灶性脑缺血再灌注损伤的保护作用 |
| The Protective Effects of Hyperbaric OxygenPreconditioning on Rats after Cerebral Ischemic Reperfusion Injuries |
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| DOI： |
| 中文关键词: 高压氧预处理 脑缺血 环氧化酶2 炎症细胞因子 丙二醛 |
| 英文关键词: Hyperbaric oxygen preconditioning Cerebral ischemia Cyclooxygenase-2 Inflammatory cytokines Malondialdehyde |
| 基金项目:广东省科技计划项目（2012A030400025） |
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| 中文摘要: |
| 目的：研究高压氧预处理对大鼠脑缺血再灌注损伤的保护作用。方法：36 只SD 大鼠随机分为假手术组、模型组及高压氧预
处理组，每组12 只。高压氧预处理组大鼠在造模前5 天给予高压氧预处理。采用线栓法建立大鼠脑缺血再灌注模型，观察高压氧
预处理对脑缺血再灌注损伤大鼠神经功能缺损评分、脑梗死面积的影响，检测大鼠缺血脑组织COX-2 mRNA和蛋白的表达以及
IL-1beta、TNF-alpha、MDA的含量。结果：高压氧预处理可明显改善脑缺血再灌注大鼠神经功能缺损评分，减少脑梗死面积，降低COX-2
mRNA 和蛋白表达量，抑制IL-1beta、TNF-alpha的表达，降低MDA 水平。结论：高压氧预处理对大鼠脑缺血再灌注损伤具有明显的保
护作用，其机制可能与抑制IL-1beta、TNF-alpha、COX-2 的表达以及减弱脂质过氧化反应有关。 |
| 英文摘要: |
| Objective:To study the protective effects of hyperbaric oxygen preconditioning on rats after cerebral ischemia
reperfusion injury.Methods:36 SD rats were randomly divided into three groups (n=12): Sham group, Model group and HBO group.
Rats in the HBO group were given continuous five days' hyperbaric oxygen preconditioning before established model. Rat's cerebral
ischemia-reperfusion model was established using the suture's method. The effect of hyperbaric oxygen preconditioning on neurological
deficit scores of rats, cerebral infarct area of rats after cerebral ischemia-reperfusion injury was investigated. The expression of COX-2
mRNA and protein as well as the content of IL-1beta, TNF-alpha and MDA in ischemic brain tissue was detected.Results:Hyperbaric oxygen
preconditioning can significantly improve neurological function of rats after cerebral ischemia and reperfusion, diminish cerebral infarct
size and reduce the amount of COX-2 mRNA / protein , inhibit the expression of IL-1beta and TNF-alpha, and decrease the level of MDA .Conclusion:HBO preconditioning has obvious protective effect on rats after cerebral ischemia-reperfusion injury, and the mechanism
may be related to its inhibition on the expression of IL-1beta, TNF-alphaand COX-2, and decrease of lipid peroxidation. |
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