为研究阿尔茨海默病(AD)异常黑胆质病证结合大鼠海马组织抗氧化酶的活性及脂质过氧化产物的浓度变化, 并观察方药对氧化应激的干预作用.选用雄性SPF级Wistar大鼠36只, 完全随机分成正常对照组、模型组、异黑颗粒高剂量干预组、异黑颗粒中剂量干预组、异黑颗粒低剂量干预组、多奈哌奇干预组.病证结合造模后3d开始药物干预15d, 行为学测试后应用紫外分光光度法检测大鼠大脑海马组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、单胺氧化酶(MAO)活性和丙二醛(MDA)含量.结果表明, 模型组大鼠海马组织SOD、GSH-Px、CAT活性明显减弱, MAO活性增强、MDA含量明显升高, 与空白对照组比较有显著性差异(P<0.01).经方药干预治疗后, 不仅生物表征有显著改善, 高剂量干预组大鼠海马组织SOD、GSH-Px、CAT活力较模型组明显提高, MAO活性减低、MDA含量明显下降, 与模型组比较有显著性差异(P<0.01), 与多奈哌奇干预组比较无明显差异(P>0.05).中剂量干预组SOD活性明显提高, 与模型组比较有显著性差异(P<0.01);GSH-Px、CAT活性提高、MAO活性降低, 与模型组比较有明显差异(P<0.05), MDA含量无明显改善, 与正常对照组比较有显著性差异(P<0.01).低剂量干预组SOD、CAT、MAO活性及MDA含量与模型组比较无显著性差异(P>0.05), 与正常对照组比较有显著性差异(P<0.01).GSH-Px活性与模型组比较有明显差异(P<0.05).由此得出, 异常黑胆质证结合双海马聚集态Aβ注射所建立的AD异常黑胆质病证结合大鼠模型, 存在明显的自由基损伤和氧化应激过度, 异常颗粒可能通过增强SOD、CAT、GSH-Px等抗氧化酶的活性, 抑制MAO活性减少单胺类神经递质的氧化分解, 抑制脂质过氧化反应而减少自由基对海马神经元损伤, 从而达到防治老年性痴呆的目的,方药高剂量疗效最突出.

In order to study the antioxidant enzyme activity of hippocampal tissue in the rat model of Alzheimer's Disease (AD) carrying abnormal savda syndrome and observe the effect and mechanism of prescription on the oxidative stress, 36 male Wistar rats are randomly divided into six groups (six rats per group). A rat model combining disease with syndrome is established, three days latter, three groups are given Yihei (abnormal savda) granula for 15 days. The spectrophoto-metric method is employed to test the activity of SOD, GSH-Px, CAT, MAO and the content of MDA in the hippocampus of rat cerebrum. It is found that.the activity of SOD, GSH-Px, and CAT is obliviously decreased, the activity of MAO and the content of MDA is significantly increased in the rat hippocampus of the model group, compared with the normal group, the difference is significant (P<0.01). After the treatment, the group given high dose of Yihei granula demonstrates that the activity of SOD, CAT, GSH-Px (P<0.01) increase, and the activity of MAO, content of MDA are decreased in rat hippocampus (P<0.01). Compared with the model group, the difference is significant (P<0.01), However, compared with Donepezil group, there is insignificant difference between these two groups (P>0.05). The group given mild dose of Yihei granula demonstrates that the activity of SOD increases, compared with the model group, the difference is significant (P<0.01). The activity of GSH-Px, CAT is increase, the activity of MAO is decrease, compared with the model group, the difference is significant (P<0.05), the content of MDA does not improve obviously, compared with normal group, the difference is insignificant (P<0.01). The group given low dose of Yihei granula is compared with the model group, there is insignificant difference in the activity of SOD, CAT, MAO, and the content of MDA(P>0.05). Compared with normal group, the difference is significant (P<0.01). There is significant difference in the activity of GSH-Px compared with model group (P<0.05). Therefore, the rat model combining disease with syndrome does an injury to free radical, oxidative stress is excessive, and Yihei granular is able to improve the activity of antioxidant enzyme, reduce the content of MDA, and inhibit the incidents of AD by antioxidative effect. It might be one of the formula mechanisms for the AD treatment.