本文選題：星形膠質(zhì)細(xì)胞 + 可塑性�。� 參考：《南京中醫(yī)藥大學(xué)》2017年碩士論文

【摘要】：研究目的觀察人參總皂苷(GTS)對皮質(zhì)酮(CORT)誘導(dǎo)的小鼠抑郁樣行為以及海馬糖原代謝和星型膠質(zhì)細(xì)胞(AS)結(jié)構(gòu)可塑性損傷的影響,探討GTS抗抑郁的作用機(jī)理。研究方法實(shí)驗(yàn)1.基于體視學(xué)技術(shù)研究抑郁模型小鼠海馬星形膠質(zhì)細(xì)胞的結(jié)構(gòu)可塑性20只C57BL/6N小鼠隨機(jī)分成2組,即對照組(Control)、模型組(CORT),每組10只。CORT組連續(xù)5周皮下注射C0RT制備小鼠抑郁模型,CORT組隨機(jī)時(shí)間點(diǎn)給予皮下注射CORT,注射劑量為20 mg · kg-1 · d-1。Control組給予相同劑量的生理鹽水。造模成功后,進(jìn)行行為學(xué)試驗(yàn)、血清CORT含量測定。將每組小鼠進(jìn)行心臟灌注后取腦,用于膠質(zhì)纖維酸性蛋白(GFAP)免疫組化染色和體視學(xué)方法定量海馬體積、GFAP陽性細(xì)胞的數(shù)目、體積和細(xì)胞突起長度。實(shí)驗(yàn)2.抑郁模型小鼠海馬組織中糖原水平的測定30只C57BL/6N小鼠隨機(jī)分成2組,即對照組(Control)、模型組(CORT),每組15只。造模成功后,將每組動物隨機(jī)分成三小組,每組5只,第一小組進(jìn)行腦糖原(GC)含量和糖原磷酸化酶-腦型(PYGM)、糖原合成酶(GS)活性的檢測。第二小組小鼠處死方法與第一組相同,取海馬組織裝入EP管中,采用Western-blot法檢測糖原磷酸化酶-腦型(PYGM)和糖原合成酶(GS)蛋白的表達(dá)。第三小組處死方法與第一組相同,取海馬組織裝入EP管中,采用Q-PCR法檢測糖原磷酸化酶-腦型(PYGM)和糖原合成酶(GS)基因水平的表達(dá)。實(shí)驗(yàn)3.GTS對抑郁模型小鼠星形膠質(zhì)細(xì)胞結(jié)構(gòu)可塑性損傷的機(jī)制研究90只C57BL/6N 小鼠隨機(jī)分成 6 組:Control、CORT、CORT+氟西汀 FLU(10mg·kg·kg-1·d-1)、CORT+低劑量組 GTSL(12.5 mg · kg-1 · d-1)、CORT+中劑量組 GTSM(25 mg · kg-1 · d-1)以及CORT+高劑量組GTSH(50 mg · kg-1 · d-1),每組15只。FLU或GTS各劑量組給予灌胃,持續(xù)21天。造模成功后在第20天和第21天分別進(jìn)行強(qiáng)迫游泳實(shí)驗(yàn)(Forced Swimming Test,FST)和強(qiáng)迫懸尾實(shí)驗(yàn)(Suspenseful Test,TST),第22天對每只小鼠進(jìn)行眼眶取血,待測血清CORT含量水平,第23天將所有動物按照實(shí)驗(yàn)要求處死。每組動物隨機(jī)分成三小組,每組5只,第一小組心臟灌注后取腦,用于GFAP免疫組化染色和體視學(xué)方法定量海馬體積、GFAP陽性細(xì)胞的數(shù)目、體積和細(xì)胞突起長度。第二小組將小鼠投入液氮中處死,取出后迅速剝離大腦,在液氮中把海馬組織研磨成粉后,取海馬組織裝入EP管中,進(jìn)行腦糖原(GC)含量和糖原磷酸化酶-腦型(PYGM)、糖原合成酶(GS)活性的檢測。第三小組小鼠處死方法與第二組相同,取海馬組織裝入EP管中,用于檢測PYGM和GS蛋白和基因的表達(dá)。實(shí)驗(yàn)4.GTS對正常小鼠星形膠質(zhì)細(xì)胞結(jié)構(gòu)可塑性損傷的機(jī)制研究20只C57BL/6N小鼠隨機(jī)分成2組:Control、GTSH組,每組10只。高劑量組GTSH(50 mg · kg-1 · d-1)給予灌胃,持續(xù)21天。造模成功后在第22天將所有動物按照實(shí)驗(yàn)要求處死。每組動物隨機(jī)分成二小組,每組5只,第一小組心臟灌注后取腦,用于GFAP免疫組化染色和體視學(xué)方法定量海馬體積、GFAP陽性細(xì)胞的數(shù)目、體積和細(xì)胞突起長度。第二小組將小鼠投入液氮中處死,取出后迅速剝離大腦,在液氮中把海馬組織研磨成粉后,取海馬組織裝入EP管中,進(jìn)行糖原含量的檢測。研究結(jié)果實(shí)驗(yàn)1.長期皮質(zhì)酮注射誘導(dǎo)小鼠抑郁樣行為,損傷海馬星形膠質(zhì)細(xì)胞結(jié)構(gòu)可塑性與Control組相比,CORT組小鼠強(qiáng)迫游泳和強(qiáng)迫懸尾的靜止時(shí)間明顯延長(P0.01),血清CORT含量顯著升高(P0.01)。小鼠海馬體視學(xué)檢測結(jié)果進(jìn)行t檢驗(yàn):①與Control組相比,CORT組小鼠海馬體積明著縮小(P0.01),GFAP陽性AS的數(shù)目顯著減少(P0.01),GFAP陽性AS的突起長度明顯縮短(P0.01)。②免疫組化GFAP染色與Control組相比,CORT組小鼠海馬GFAP陽性AS的體積明顯縮小(P0.01)。實(shí)驗(yàn)2.長期皮質(zhì)酮注射下調(diào)海馬組織中糖原的水平與Control組相比,CORT組小鼠海馬GC含量顯著降低(P0.01),海馬PYGM活性顯著升高(P0.01),海馬GS活性顯著升高(P0.01)。與Control組相比,CORT組小鼠海馬GS蛋白含量表達(dá)顯著升高(P0.01),海馬PYGM蛋白含量表達(dá)顯著升高(P0.01),海馬GS基因含量表達(dá)顯著升高(P0.01),海馬PYGM基因含量表達(dá)顯著升高(P0.01)。實(shí)驗(yàn)3.GTS可上調(diào)抑郁模型小鼠海馬組織中糖原的水平,拮抗星形膠質(zhì)細(xì)胞結(jié)構(gòu)可塑性的損傷CORT組血清皮質(zhì)酮水平高于Control組(P0.01),造模期間給予各劑量GTS對血清皮質(zhì)酮水平均無顯著影響。FLU、GTS 3個(gè)劑量組均能明顯拮抗模型小鼠的FST和TST(均P0.01),以及縮短靜止不動時(shí)間,并顯著性抑制模型小鼠海馬PYGM的活性(P0.05,P0.01、P0.05、P0.05)。與CORT組相比,FLU、GTSL、GTSH組均能顯著上調(diào)模型小鼠海馬組織GC含量(均P0.01)。與CORT組相比,FLU、GTSM、GTSH組均能顯著上調(diào)模型小鼠海馬組織GS的活性(均P0.01),顯著拮抗模型小鼠海馬組織內(nèi)PYGM蛋白的表達(dá),均P0.01),且顯著下調(diào)模型小鼠海馬組織內(nèi)PYGM基因的表達(dá)(均P0.01)。與CORT組相比,FLU、GTSM、GTSH組均能顯著上調(diào)模型小鼠海馬組織內(nèi)GS蛋白的表達(dá),且顯著上調(diào)模型小鼠海馬組織內(nèi)GS基因的表達(dá)(P0.05,p＜0.05,P0.01)。與CORT組比,FLU、GTSM、GTSH組的模型小鼠海馬體積明顯增大(均P0.01),海馬GFAP陽性細(xì)胞數(shù)目明顯增加(均P0.01)。與CORT組比,FLU、GTSH組的模型小鼠海馬GFAP陽性AS的體積增大(均P0.05),海馬GFAP陽性AS的突起長度顯著增加(均P0.01)。實(shí)驗(yàn)4.GTS不影響正常小鼠海馬星形膠質(zhì)細(xì)胞的結(jié)構(gòu)可塑性每組每只小鼠海馬體視學(xué)檢測結(jié)果進(jìn)行t檢驗(yàn):①與Control組相比,海馬GC含量水平無明顯變化(P0.05)。②與Control組相比,GTSH組小鼠海馬體積無明顯變化(P0.05),海馬GFAP陽性AS的數(shù)目無明顯變化(P0.05),海馬GFAP陽性AS的體積無明顯變化(P0.05),海馬GFAP陽性AS的突起長度無明顯變化(P0.05),研究結(jié)論本實(shí)驗(yàn)采用長期CORT注射模擬慢性應(yīng)激,復(fù)制抑郁動物模型,觀察GTS抗抑郁的作用,并從海馬糖原代謝和星形膠質(zhì)細(xì)胞結(jié)構(gòu)可塑性角度探討機(jī)制。研究結(jié)果顯示長期C0RT能誘導(dǎo)抑郁樣行為并損傷海馬星形膠質(zhì)細(xì)胞結(jié)構(gòu)可塑性。GTS抗抑郁作用有如下特點(diǎn):①具有抗抑郁樣行為作用,如通過行為學(xué)FST和TST實(shí)驗(yàn),高劑量GTS能減少皮質(zhì)酮抑郁模型小鼠的抑郁樣行為。②通過增加AS內(nèi)糖原含量拮抗海馬損傷。③上調(diào)皮質(zhì)酮抑郁模型小鼠海馬組織內(nèi)GS蛋白和基因表達(dá)、下調(diào)皮質(zhì)酮抑郁模型小鼠海馬組織內(nèi)PYGM蛋白和基因表達(dá),表明高劑量GTS可使糖原在蛋白和基因水平上同時(shí)增加。④提高小鼠海馬體積、GFAP陽性細(xì)胞數(shù)目、GFAP陽性細(xì)胞的細(xì)胞體積、GFAP陽性細(xì)胞的突起長度,改善海馬AS可塑性。本研究認(rèn)為,GTS抗抑郁的作用可能與改善AS的糖原含量和結(jié)構(gòu)可塑性有關(guān)。
[Abstract]:Objective To observe the effect of Panax ginseng total saponins (GTS) on the depressive behavior of mice induced by corticosterone (CORT), the effect of hippocampal glycogen metabolism and the structural plasticity of astrocytes (AS), and to explore the mechanism of GTS antidepressant action. Method 1. study method experiment based on stereology to study the structure of astrocytes in the hippocampus of depressive model mice 20 C57BL/6N mice were randomly divided into 2 groups, that is, the control group (Control), the model group (CORT), each group of 10.CORT groups was injected with C0RT for 5 weeks to prepare the mice depression model, and the CORT group was given the subcutaneous injection of CORT at random time point, and the injection amount was 20 mg. Kg-1 d-1.Control group given the same dose of saline. Behavior test and determination of serum CORT content. The brain was taken after heart perfusion in each group. The volume of hippocampus, the number of GFAP positive cells, volume and the length of cell protuberance were quantified by immunohistochemical staining and stereological method of glial fibrillary acidic protein (GFAP). The level of glycogen in hippocampus of experimental 2. depressed model mice was measured by 30 C5 7BL/6N mice were randomly divided into 2 groups, namely, the control group (Control), the model group (CORT), 15 in each group. After the success of the model, each group was randomly divided into three groups, each group was 5. The first group was tested for the content of brain glycogen (GC), glycogen phosphorylase brain (PYGM), and glycogen synthase (GS) activity. The second group mice were killed in the same way as the first group. The expression of glycogen phosphorylase brain type (PYGM) and glycogen synthetase (GS) protein was detected by Western-blot method. The third group was killed in the same way as the first group. The hippocampal tissue was loaded into the EP tube, and the expression of glycogen phosphorylase brain (PYGM) and glycogen synthetase (GS) gene was detected by Q-PCR. 90 C57BL/6N mice were randomly divided into 6 groups: Control, CORT, CORT+ fluoxetine FLU (10mg. Kg-1 D-1), CORT+ low dose group GTSL (12.5), and high dose group (50). Kg-1. D-1), each group of 15.FLU or GTS dose groups were given the gastric lavage for 21 days. After the success of the model, the forced swimming test (Forced Swimming Test, FST) and the forced tail suspension experiment (Suspenseful Test, TST) were performed respectively, and the blood of each mouse was taken into the orbit for twenty-second days, and the level of the serum CORT content was measured, and the twenty-third days would be done. Animals were killed in accordance with the experimental requirements. Each group of animals was randomly divided into three groups, each group was 5. After the first group of heart perfusion, the brain was taken. GFAP immunohistochemical staining and stereological methods were used to quantify the volume of the hippocampus, the number of GFAP positive cells, the volume and the length of the cell protuberance. The second group killed the mice in liquid nitrogen and quickly stripped off. After grinding the hippocampus into powder in the liquid nitrogen, the hippocampus was loaded into the EP tube to detect the content of GC and the activity of glycogen phosphorylase brain (PYGM) and glycogen synthase (GS). The third group of mice were executed in the same way as the second groups, and the hippocampus group was woven into the EP tube to detect the expression of PYGM and GS proteins and genes. Study the mechanism of plastic damage of astrocyte structure in normal mice by experimental 4.GTS, 20 C57BL/6N mice were randomly divided into 2 groups: Control, group GTSH, 10 in each group. GTSH (50 mg. Kg-1. D-1) was given to the stomach for 21 days in the high dose group. All the animals were killed at twenty-second days after the model was successful. The animals of each group were randomly divided into two groups. The two group, each group of 5, the first group after heart perfusion to take the brain, used for GFAP immunohistochemical staining and stereological methods to quantify the volume of hippocampus, the number of GFAP positive cells, volume and cell protuberance length. Group second killed the mice in liquid nitrogen, removed the brain quickly, and ground the hippocampus into powder in liquid nitrogen and took the hippocampus. The tissue was loaded into EP tube to detect the content of glycogen. Results 1. a long-term corticosterone injection induced depressive behavior in mice. Compared with the Control group, the plasticity of hippocampal astrocytes was significantly longer than that of the Control group (P0.01), and the serum CORT content was significantly increased (P0.01). The results of t test in rat hippocampus: (1) compared with group Control, the volume of hippocampus in CORT group was reduced (P0.01), the number of GFAP positive AS decreased significantly (P0.01), and the length of GFAP positive AS significantly shortened (P0.01). 0.01) in experiment 2., compared with group Control, the level of glycogen in hippocampus of long-term corticosterone injection was significantly decreased (P0.01), PYGM activity in hippocampus was significantly increased (P0.01) and hippocampal GS activity increased significantly (P0.01). Compared with group Control, the expression of GS protein in hippocampus of CORT mice increased significantly (P0.01), hippocampus The expression of protein content increased significantly (P0.01), the expression of GS gene content in hippocampus was significantly increased (P0.01), and the expression of PYGM gene in hippocampus increased significantly (P0.01). Experimental 3.GTS could increase the level of glycogen in the hippocampus of depression model mice, and antagonize the plasticity of astrocytes in the CORT group, the serum corticosterone level was higher than that of the Control group (P0.01). Every dose of GTS had no significant effect on the level of serum corticosterone during the process of modeling.FLU, and the 3 doses of GTS could obviously antagonize the FST and TST of the model mice (all P0.01), and shorten the resting time, and significantly inhibit the activity of PYGM in the hippocampus of the model mice (P0.05, P0.01, P0.05, P0.05). The content of GC in hippocampus of model mice was increased (P0.01). Compared with group CORT, FLU, GTSM and GTSH could significantly increase the activity of GS in the hippocampus of model mice (P0.01), significantly antagonize the expression of PYGM protein in the hippocampus of model mice, all P0.01), and significantly down the expression of PYGM gene in the hippocampus of model mice. Compared with the group FLU, GTSM and GTSH, the expression of GS protein in the hippocampus of the model mice was significantly up-regulated, and the expression of GS gene in the hippocampus of the model mice was significantly increased (P0.05, P < 0.05, P0.01). Compared with the CORT group, FLU, GTSM, the hippocampal volume of the model mice of the GTSH group increased significantly (all of them). 1). Compared with group CORT, the volume of GFAP positive AS in hippocampus of model mice of FLU and GTSH increased (P0.05), and the protuberance length of hippocampal GFAP positive AS increased significantly (all P0.01). Experimental 4.GTS did not affect the structural plasticity of astrocytes in the hippocampus of normal mice. There was no significant change in the level of hippocampal GC content (P0.05). Compared with the Control group, there was no significant change in the volume of hippocampus in the GTSH group (P0.05), the number of GFAP positive AS in the hippocampus was not significantly changed (P0.05), and the volume of the GFAP positive AS in the hippocampus was not significantly changed (P0.05), and there was no obvious change in the length of the hippocampal positive AS. The conclusion of the study was adopted in this experiment. Long term CORT injection simulated chronic stress, replicated depressive animal model, observed the antidepressant effect of GTS, and explored the mechanism of hippocampal glycogen metabolism and astrocyte structural plasticity. The results showed that long-term C0RT could induce depressive behavior and damage the antidepressant effect of hippocampus astrocytic structure plastic.GTS as follows. Points: (1) it has antidepressant behavior, such as through the behavior FST and TST experiments, high dose GTS can reduce the depressive behavior of the corticosterone depression model mice. (2) antagonize the hippocampus injury by increasing the content of glycogen in AS. (3) up regulation of GS protein and gene expression in the hippocampus of corticosterone depression model mice, and down-regulation of corticosterone depression model mice The expression of PYGM protein and gene in the hippocampus indicates that high dose of GTS can increase glycogen at the level of protein and gene. 4. Increase the volume of the hippocampus, the number of GFAP positive cells, the cell volume of the GFAP positive cells, the protuberance length of the GFAP positive cells, and improve the plasticity of AS in the hippocampus. This study suggests that the antidepressant effect of GTS may be modified by the modification of GTS. The glycogen content of good AS is related to the plasticity of the structure.

【學(xué)位授予單位】：南京中醫(yī)藥大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R285.5

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