丁香酚吸嗅对MCAO模型大鼠脑源性神经营养因子的影响

Effect of Eugenol inhalation on brain derived neurotrophic factor in SD rats MCAO model

目的研究丁香酚吸嗅对MCAO模型SD大鼠认知和记忆能力的行为学的影响,评价其对脑缺血后再灌注损伤的干预作用及其可能的作用机制。方法将80只SD雄性大鼠,随机分为正常组、模型组、丁香酚组和假手术组,每组20只。采用大脑中动脉内线栓阻断法(MCAO)制造大鼠局灶性脑缺血再灌注模型,缺血2 h后再灌注24 h。给予相应处理3 w后,大鼠行神经行为学评分后处死,取大脑行2,3,5-氯化三苯基四氮唑(TTC)染色,计算脑梗死容积百分比;Morris水迷宫实验检测学习记忆能力;并利用免疫组织化学染色法观察脑源性神经营养因子(BDNF)在海马CA3区的表达。结果丁香酚吸嗅组干预3 w后与模型组比较神经功能评分差异有显著性(P<0.01);TTC染色梗死面积明显减少(P<0.01),Morris水迷宫实验差异有显著性(P<0.05);海马CA3区BDNF的表达显著性增多。结论丁香酚吸嗅对MACO模型大鼠的损伤有明显的保护作用,其机制可能是提高脑内BDNF含量,调节脑区功能,从而达到对脑缺血再灌注损伤的防治作用。

Objective It is designed to research and evaluate the effects of eugenol treatment through olfactory pathway on cognitive and memory behavior caused by MCAO model of SD rat,to evaluate the intervention of brain ischemiareperfusion injury,and to explore the possible underlying mechanism. Methods 80 SD male rats were randomly divided into normal group,model group,eugenol group and control group,with each group of 20 rats. We used the bolt inside the middle cerebral artery occlusion（ middle cerebral artery occlusion,MCAO） manufactured after focal cerebral ischemia-reperfusion model,focal ischemia was achieved by middle cerebral artery occlusion（ MCAO） on the right side for 2 h. After24 h of reperfusion,giving corresponding treatment 3 weeks later,rats were sacrificed after neurobehavioral score were tested; The brain tissue were stained with 2,3,5-triphenyl tetrazolium chloride（ TTC）,the cerebral infarction volume percentage was calculated; We used the Morris water to detect learning and memory ability; Immunohistochemical staining was used to observe the expression of brain-derived neurotrophic factor（ BDNF） in the hippocampus CA3 area. Results The nerve function score of eugenol group after the intervention of 3 week（ P 〈0. 01）; the infarction area of TTC staining was significantly reduced（ P 〈0. 01）; Morris water test（ P 〈0. 05）; the expression of BDNF significantly increased in hippocampal CA3 area. Conclusion The eugenol treatment through olfactory pathway on MACO model rats has a obvious protective effect,its mechanism may improve the levels of BDNF in the brain,regulate brain function,to achieve the prevention and treatment of cerebral ischemia-reperfusion injury.