摘要
目的构建β-淀粉样肽(1-40)(Aβ1-40)联合D-半乳糖(D-gal)致痴呆模型,探讨天麻素抗氧化的分子机制。方法成年雄性SD大鼠36只,侧脑室注射Aβ1-40联合腹腔注射D-gal构建SD大鼠痴呆模型,并同时给予天麻素预防性治疗,采用Morris水迷宫实验(MWM)进行行为学检测,用化学比色法检测大脑皮质过氧化氢(H2O2)及还原型谷胱甘肽(GSH)和谷胱甘肽还原酶(GR)的含量。用免疫印迹法检测大脑皮质中p38和P-p38的含量。结果痴呆模型组与对照组比较:逃避潜伏期明显延长(P<0.05),在第Ⅲ象限逗留的时间明显减少(P<0.05),跨越平台次数明显减少(P<0.05),皮质H2O2的含量增加,皮质GSH和GR的含量降低(P<0.05),P-p38表达增加(P<0.05);而天麻素治疗后:与痴呆模型组相比,大鼠逃避潜伏期明显缩短(P<0.05),在第Ⅲ象限逗留的时间明显增加(P<0.05),跨越平台次数明显增加(P<0.05),皮质H2O2的含量减少,皮质GR和GSH的含量升高(P<0.05),P-p38表达减少(P<0.05)。p38的表达在3组之间无差异(P>0.05)。结论天麻素影响了痴呆模型大鼠皮质部分内源性巯醇抗氧化物(酶)如GSH和GR的含量,抑制了H2O2的产生,影响了P-p38的表达,对改善学习记忆能力,对抗大鼠神经系统的退行性变有一定的作用。
Objective To established β-amyloid peptide（1-40） （Aβ1-40） and D-galactose（D-gal） AD rat models and to explore the anti-oxidation molecular mechanism of the Gastrodin and provide the experimental foundations for clinical treatment of AD. Methods AD rat models were established by lateral ventricle injection of Aβ1-40 and abdominal cavity injection of D-gal（ 100 mg/kg） to thirty six male SD rats. Meantime, the rats were treated by intragastric administration the Gastrodin. Then the behavioral testing of experimental rats was performed by the Morris water maze （ MWM）. The thiol antioxidants including hydrogen peroxide （ H2O5 ）, glutathione reductasc （GR） and glutathion （ GSH ） activities were examined by colorimetric method. The concentration of the p38 and P-p38 was examined respectively by Western blotting. Results The AD model rats when compared with control group exhibited a significant increase in escape latencies（P 〈 0. 05） , and a decrease in the time of staying at the third quadrants of platform and the degree of crossing over a platform. The cerebral cortex concentration of the H2O2 was increased, and the concentrations of the GR and GSH were decreased（P 〈0.05 ）. The expression of P-p38 was increased（ P 〈 0. 05 ）. After the treatment with Gastrodin, the AD model rats exhibited a significant decrease in escape lateneies （P 〈 0.05） , an obvious increase in the time of staying the third quadrants of platform （ P 〈 0. 05） and the increase of crossing over a platform （ P 〈 0. 05 ） when compared with the AD group （ P 〈 0.05 ）. The concentration of the H2O2was decreased, the concentrations of GR and GSH were increased （ P 〈 0.05 ）. The expression of the P-p38 was less than that of the AD model （ P 〈 0. 05）. But there were no significant differences between the three groups in the expression of the p38 （P 〉 0.05 ）. Conclusion Gastrodin could improve the orientedlearning and memory capacity and prevent the neurodegeneration
出处
《解剖学报》
CAS
CSCD
北大核心
2010年第4期485-490,共6页
Acta Anatomica Sinica
基金
国家自然基金资助项目(30860336)
云南省科技厅-昆明医学院联合资助项目(2007C0005R
2008CD053)
云南省中青年学术和技术带头人后备人才培养项目(2009CI033)
