摘要
目的探讨复脑汤在反复脑缺血再灌注损伤中的神经保护机制.方法实验分为空白对照组、假手术组、模型组和复脑汤组.实验期间空白对照组、假手术组和模型组以蒸馏水灌胃,复脑汤组以复脑汤灌胃,用药5d后实施脑缺血再灌注术.手术后第1,10日,小鼠断头取脑测定超氧化物歧化酶(SOD)的活性以及丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的含量.结果与对照组(26.82±3.58)mg/g相比,模型组鼠脑缺血再灌注后SOD活性第1日(13.95±4.52)mg/g和第10日(15.82±4.39)mg/g明显降低,MDA,TNF-α,IL-1β含量显著升高.与模型组相比,复脑汤能显著提高SOD[(21.35±4.07)mg/g]的活性(F=16.56,q=3.29,P<0.05),并降低MDA的水平(F=81.88,q=34.61,P<0.01).复脑汤组能显著下调小鼠大脑皮质TNF-α(F=96.44,q=35.11,P<0.01)和IL-1β(F=38.30,q=40.92,P<0.01)的水平.结论复脑汤通过降低脑缺血再灌注后脑氧化反应以及TNF-α和IL-1β表达而起到神经保护作用.
AIM： To investigate the neuroprotective mechanism of Funao decoction in the treatment of repeated cerebral ischemia/ reperfusion injury. METHODS： Totally 70 mice were randomly divided into 7 groups of 10 mice each： blank control group, sham operated groups of 1 and 10 d, model groups of 1 and 10 d, herb groups of 1 and 10 d （ Funao decoction）. The mice in the herb groups were perfused gastrically with Funao decoction, while those in the other groups with distilled water, both followed by cerebral ischemia/reperfusion 5 d later. One or 10 d after operation, the brains were taken following rapid decapitation to measure the activity of superoxide dismutase （SOD） and the contents of malondialdehyde （ MDA）, tumor necrosis factor-α （ TNF-α） and interleukin-1β （IL-1β）. RESULTS： The activities of SOD were significantly reduced to （ 13.95 ± 4.52） mg/g and （ 15.82 ± 4.39） mg/g respectively at 1 and 10 d after cerebral isehemia/ reperfusion, as compared with the control group [ （26. 82 ± 3.58） mg/g] ; while the contents of MDA, TNF-α and IL-1β were significantly increased. In comparison with the model group, Funao decoction was effective to increase the activity of SOD [（21.35±4.07） mg/g, F=16.56, Q=3.29, P〈0.05] and decrease the contents of MDA （F = 81. 88, Q =34. 61,P 〈 0.01 ）. Funao decoction played a down-regulative role in the contents of TNF-α and IL-1β （F =96.44,Q =35.11 ,P 〈0.01 ; F= 38.30,Q =40.92, P 〈0. 01 ）. CONCLUSION： Funao decoction plays a neuroproteetive role against the repeated isehemia/ reperfusion injury through reducing the oxidation and down-regulating the expressions of TNF-α and IL-1β in the brain.
出处
《第四军医大学学报》
CAS
北大核心
2006年第19期1758-1760,共3页
Journal of the Fourth Military Medical University
基金
陕西省科技攻关项目(2002K10-J6)
