改良三甲散对AD大鼠细胞模型相关信号通路的调节作用  

The Regulation of Gai Liang San Jia San in the Signaling Pathway of AD Cell Model on Rats

作　　者：刘学凤[1] 张赓[1] 刘涛[1] 

机构地区：[1]南京中医药大学基础医学院,江苏南京210023

出　　处：《时珍国医国药》2015年第10期2305-2307,共3页Lishizhen Medicine and Materia Medica Research

基　　金：国家自然科学基金(No.81173313)

摘　　要：目的探讨改良三甲散对AD大鼠细胞模型NF-κB和JNK信号传导通路的调节作用。方法选用健康大耳白兔分高、中、低剂量连续6天给药,抽取含药脑脊液备用。选用出生24 h内乳大鼠取海马神经细胞做原代培养,采用终浓度为5μmol/L的Aβ25-35诱导造模,用改良三甲散含药脑脊液处理AD细胞模型,采用ELISA测定细胞上清液中NF-κB和JNK的表达情况。结果改良三甲散能显著降低细胞模型上清液中NF-κB和JNK的含量(P<0.05)。结论改良三甲散治疗老年性痴呆病的机制可能与抑制NF-κB和JNK信号转导通路的激活有关。Objective To discuss the regulation of Gai Liang San Jia San in NF- κB and JNK signaling pathway of AD cell model on rats. Methods Choosing healthy rabbits,divided into high,medium and low dose group,6 days administered continuously,then extract the drug- containing cerebrospinal fluid backup. Choosing neonatal rat within 24 hours of birth,taking hippocampal neurons for primary culture. Modeling using Aβ25- 35 which final concentration is 5μmol / L. Treating AD cell model with drug-containing cerebrospinal fluid. Determining the expression of NF- κB and JNK in cell supernatant. Results Gai Liang San Jia San can significantly reduce the content of NF- κB and JNK in cell model supernatant（ P〈0. 05）. Conclusion Mechanism of Gai Liang San Jia San in treatment of Alzheimer＇s disease may concerning inhibition of NF- κB and JNK signal transduction pathway activation.

关 键 词：改良三甲散 AD NF-κB JNK 

分 类 号：R277.7[医药卫生—中医学] R289