摘要
目的观察旋覆花内酯（l-O-acetylbfitannilactone，ABL）对Aβ25-35海马内注射所致阿尔采末病（Alzheimers disease，AD）模型大鼠海马环加氧酶2（COX-2），核转录因子KB（NF-kB）表达的影响，探讨其对AD大鼠的治疗作用及机制。方法30只SD大鼠随机分为对照组、模型组及药物处理组，Aβ25-35海马内注射制备AD大鼠模型，药物处理组给予ABL26mg·kg^-1·d^-1，模型组给予等量溶剂，分两次灌胃，共21d。用Morris水迷宫测定大鼠的学习记忆能力，免疫组化及Western blot测定大鼠海马COX-2，NF-kB蛋白表达。结果AD大鼠在定位航行试验中，逃避潜伏期延长，单位时间内跨越原平台次数减少，空间记忆力受损，与对照组及药物处理组大鼠比较差异有统计学意义（P〈0．05）；于试验d2、3、4药物处理组与对照组大鼠比较差异无统计学意义（P〉0．05）。模型组海马COX-2、NF-kB表达升高（P〈0．05），分别是对照组的2．8倍和1．6倍，药物处理组COX-2、NF—kB表达下降，与模型组比较差异有统计学意义（P〈0．05）。结论ABL的抗炎作用可能是其改善AD大鼠学习记忆能力的作用机制之一。
Aim To explore the molecular mechanism of ABL in rats with AD. Methods Aβ25-35 was injected into bilateral hippocampus to create AD model. Rats were administered by gavage with ABL of 26 mg ·kg^-1·d^-1 for 3 weeks to determine the protective and therapeutic effects on treatment rats. Morris water maze was used to examine spatial and memory performance of rats. The cyclo-oxygenase-2（COX-2） and nuclear factor-kB （NF-kB） protein in hippocampus were detected by immunohistochemistry and Western blot. Results AD model rats displayed spatial and memory impairment shown by longer escape latency and less frequency of trying to find the platform （ P 〈 0. 05 ）. ABL treatment improved learning and memory of rats with AD and average escape latency between ABL-treated and control rats showed no difference （ P 〉 0. 05 ）. Levels of COX-2 and NF-kB in hippocampus increased approximately 2.8 and 1.6 folds respectively in AD model tats than in those of rats with sham operation （ P 〈 0. 05 ）, but no differences in levels of COX-2 and NF-kB were found between ABL-treated and control rats （ P 〉 0. 05 ）. Conclusion The preventive and therapeutic effects of ABL on rats with AD was related to the degression of COX-2 and NF-kB expression.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第4期437-440,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30472167)
河北省自然科学基金资助项目(NoC2005000722)
