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Explore The Reshape Mechanism Of Dysthymia Rat Hippocampal Cells By The Methods Of Shuganliqitiaoshen Based On The Expression Of BDNF And TrkB After Receptor

Posted on:2015-02-15Degree:MasterType:Thesis
Country:ChinaCandidate:P LiFull Text:PDF
GTID:2284330467951103Subject:Chinese medical science
Abstract/Summary:PDF Full Text Request
Purpose: This study by observing each dysthymia diseases with ease the weight andbehavior before and after the experiment in rats, the hippocampus brain derived neurotrophicfactor, BDNFmRNA, tyrosine kinase receptor B, pathology and other indicators of change, toexplore Chinese medicine KeyuShushen particles of dysthymia rat hippocampal nerve cellsreshape mechanism.Method:1. Chronic unpredictable mild stimulation and solitary for the method toestablish dysthymia depression of liver-QI rat model.2. The observation group (blank group, model group, the fluoxetine group, KeYushushenparticles high dose group (hereinafter referred to as "high dose group"), KeYushushenparticles dose group (hereinafter referred to as "dose group"), KeYushushen particles low dosegroup (hereinafter referred to as the low dose group)) rat body weight, sugar waterconsumption, Open-field test and behavioral changes.3. By reverse transcription polymerase chain reaction assays BDNFmRNAproteinexpression levels, using immunohistochemical method to observe the hippocampus BDNF,TrkBpositive cells expression changes.4. The application of electron microscope in the rat hippocampal neurons, synapticultrastructure changes.Result:1. Compared with the blank group, the determination of the prescribed date eachrat body weight, water consumption reducing sugar, Open-field test score decreased,especially in the model group, the most obvious change.2. Compared with the blank group, each group of rats BDNFmRNAprotein expressionwere lower, compared with model group, high dose, fluoxetine group protein expressionsignificantly raised (P <0.01).3. BDNF, TrkBstatistical results showed that the positive cells expressed positive cells inthe area of comparison: compared with blank group, each group rats then BDNF, TrkBarea ofpositive cells were decreased (P <0.01), compared with model group, high dose, fluoxetinegroup of positive cells increased significantly (P <0.01). Grey value minimum average greyvalue comparison, blank group, followed by high dose and fluoxetine group, is once again in the dose and low dose, model group grey value is highest.4. Then observe the hippocampus neurons of BDNF, TrkBcells: positive cells expressioncharacterized by tan particles composed, expressed in C1, C3area clear. Blank group ofnormal cell structure, obvious positive expression. Model group cell shrinkage, or edema andnecrosis. Each treatment group cell positive expression level between gaps in the model group,the fluoxetine group and high dose group of cell structure and the degree of positiveexpression is better than that of low dose, middle dose group.5. Under electron microscopy observation of hippocampal cells form and blank group ofneurons is normal, nucleoli, nuclear periplasm abundant organelles. Some mild dense shapedmodel group neurons, nuclear membrane and local owed clear, nuclear matrix density withinperiplasm. The rest of the four groups treatment group of neurons and neural felt changebetween normal group and model group. Fluoxetine group and high dose group is the mostclose to the normal group, the second dose, low dose group.Conclusion:1. The dysthymia depression of liver-QI rat model establish success.2. Chinese medicine KeYushushen particles and fluoxetine can improve dysthymia ratbehavior.As effective as high dose of Chinese medicine and fluoxetine.3. KeYushushen particles can increase BDNFmRNAprotein expression, promotion ofBDNF and TrkBnerve cell regeneration, this drug is reshaping effect for BDNF, TrkBcells.4. KeYushushen particles on the treatment of dysthymia rat at least by reshaping ofBDNF, TrkB cells and play a role.
Keywords/Search Tags:the methods of ShuGanliqitiaoshen, Dysthymia, liver-QI, BDNFmRNABDNF, TrkB, nerve cells reshape
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