Effect Of Yizhi Jiannao Granule Concentration Fluid (YCF) On The Expression Of Pin1,HMGB1 MRNA In The Hippocampus Of Senescence Accelerated Mouse SAMP8

Objective:Through researching the effection of yizhi jiannao granule concentration fluid(YCF)on the expression of peptidy 1-prolyl -cis- trans isomerase A(Pin1)mRNA and high mobility group box 1(HMGB1)mRNA in the hippocampus of Senescence Accelerated Mouse SAMP8,this work discusses partially the mechanism of traditional Chinese medicine YCF with respect to its effectiveness to treat Alzheimer's disease.Methods:Six--month old SAMP8 mice were randomly divided into the YCF group and model group after the Morris water maze pre-screen testing.Six--month old SAMR1 mice were served as a normal control group,the YCF group was gavaged YCF,the model group and normal control group were gavaged double-distilled water for 8 weeks, the hippocampus were taken out to examine the expression of Pin1,HMGB1 mRNA by semi-quantitative RT-PCR.Results:1.The SAMP8 mice had significantly decreased in ability o f learning and memory than the SAMR1 mice(the longer escape latency,the more times in platform quadrant)2.In the model group,the level of Pinl mRNA decreased Compared with the normal control group(P＜0.05),in the YCF group the level of Pinl mRNA increased Compared with the model group(P＜0.05).In the model group,the level of HMGB1 mRNA increased Compared with the normal control group(P＜0.05),in the YCF group the level of HMGB1 mRNA decreased Compared with the model group(P＜0.05);while the YCF group and normal control group had no significant difference.Conclusion:1.SAMP8 is reliable as a animal model of Alzheimer's.2.The decreased level of Pin1 mRNA and the increased level of HMGB1 mRNA in the SAMP8 mice,which probably is part of pathology of Alzheimer's disease.3.Yizhi jiannao granule can protect neurons,reduce amyloid plaques and nerve fibers tangles through increacing the Pin1 level and decreacing the HMGB1 level to treat Alzheimer's disease.That showing Yizhi jiannao granule has multitarget mechanism of AD.