本文選題：海馬 + 雌激素　； 參考：《第三軍醫(yī)大學(xué)》2017年碩士論文

【摘要】：研究報(bào)道隨著年齡的逐漸增長(zhǎng),老化所引起的雌激素(estrogen,E_2)水平降低在癡呆癥如阿爾茲海默病(Alzheimer’s disease,AD)的學(xué)習(xí)記憶方面扮演著重要的角色。目前,AD的具體發(fā)病機(jī)制仍未完全明確,現(xiàn)有的治療方案療效并不理想。因此,研究探索AD的發(fā)病機(jī)理和治療方法對(duì)于預(yù)防和治療AD,促進(jìn)醫(yī)療護(hù)理和家庭照護(hù)都具有深遠(yuǎn)的影響。E_2不僅可以影響女性的生理發(fā)育,還在改善老年的記憶力衰退方面也具有積極的作用,在調(diào)控海馬突觸可塑性以及學(xué)習(xí)記憶的調(diào)節(jié)過(guò)程中需要借助雌激素受體(estrogen receptor,ER)的參與來(lái)產(chǎn)生作用。E_2的受體分為兩大類:一類是膜受體GPR30,位于細(xì)胞內(nèi)的膜性成分包括細(xì)胞膜、線粒體膜、內(nèi)質(zhì)網(wǎng)等,通過(guò)第二信使途徑介導(dǎo)E_2對(duì)某些生理功能的調(diào)節(jié);另一類是經(jīng)典的核受體,包括雌激素α受體(estrogen receptorα,ERα)和雌激素β受體(estrogen receptorβ,ERβ),它們主要在細(xì)胞核內(nèi)通過(guò)與DNA結(jié)合從而調(diào)節(jié)靶基因的轉(zhuǎn)錄。類固醇受體輔助活化因子-1(steroid receptor coactivator-1,SRC-1)作為是促進(jìn)核受體調(diào)節(jié)靶基因轉(zhuǎn)錄活動(dòng)所必需的輔助因子之一,高表達(dá)于海馬、大腦皮層等腦區(qū),其表達(dá)受產(chǎn)后發(fā)育和性腺切除的影響。有研究表明在給予卵巢切除手術(shù)和核受體抑制劑處理后海馬突觸蛋白表達(dá)和突觸及樹(shù)突棘密度明顯下降,雌激素替代治療及其核受體激動(dòng)劑可以增加突觸蛋白的表達(dá)和樹(shù)突棘的密度,但ERβ在當(dāng)中的作用機(jī)制目前尚不明確。ERβ克隆于1996年,過(guò)去20年的研究發(fā)現(xiàn)ERβ在多種動(dòng)物的體內(nèi)均有較為廣泛的表達(dá),并且參與了E_2對(duì)多種腦功能作用的調(diào)節(jié),且在不同的分區(qū)其表達(dá)分布和功能作用也不盡相同。在中樞神經(jīng)系統(tǒng)內(nèi),大腦皮層、海馬等區(qū)域有大量ERβ的表達(dá),提示ERβ可能扮演著介導(dǎo)E_2調(diào)控學(xué)習(xí)記憶的功能性受體的角色。在生殖系統(tǒng),睪丸、卵巢等組織器官內(nèi)可檢測(cè)到ERβ的存在,它可能參與E_2調(diào)節(jié)生殖細(xì)胞的生長(zhǎng)、分化等過(guò)程。另外,在心血管、消化道等系統(tǒng)內(nèi)也可檢測(cè)到ERβm RNA,并且也具有十分重要生理意義。腦內(nèi)的研究發(fā)現(xiàn),利用ERβ特異性拮抗劑以及基因敲除等方法抑制ERβ后,發(fā)現(xiàn)海馬突觸蛋白表達(dá)顯著下降,樹(shù)突棘密度降低,出現(xiàn)空間學(xué)習(xí)記憶障礙。通過(guò)ERβ激動(dòng)劑活化ERβ可改善突觸可塑性和提高空間學(xué)習(xí)記憶,提示ERβ對(duì)學(xué)習(xí)記憶有著重要的調(diào)控作,但是其具體機(jī)制尚不清楚。肌動(dòng)蛋白(actin)是構(gòu)成細(xì)胞骨架的重要成分,actin聚合與解聚的動(dòng)態(tài)變化是突觸可塑性的基礎(chǔ),也是學(xué)習(xí)記憶的基礎(chǔ)。球狀肌動(dòng)蛋白(即G-actin)在Profilin-1等分子的誘導(dǎo)下聚合成為螺旋狀的肌動(dòng)蛋白(F-actin)。因此,F-actin/G-actin比例的變化常作為衡量的肌動(dòng)蛋白聚合程度的指標(biāo)。研究還發(fā)現(xiàn)哺乳動(dòng)物雷帕霉素靶蛋白復(fù)合體2(mammalian target of rapamycincomplex 2,m TORC2)對(duì)actin細(xì)胞骨架的聚合有著重要的調(diào)節(jié)作用,敲除m TORC2的核心成分Rictor導(dǎo)致actin聚合程度與樹(shù)突棘密度下降,并導(dǎo)致嚴(yán)重的學(xué)習(xí)記憶障礙,而直接激活Rictor的效應(yīng)分子p-AKT(AKT ser473)可逆轉(zhuǎn)上述學(xué)習(xí)記憶障礙,證明m TORC2在調(diào)節(jié)actin細(xì)胞骨架聚合與學(xué)習(xí)記憶中的重要作用。既往研究報(bào)道ERβ可調(diào)節(jié)樹(shù)突棘密度和學(xué)習(xí)記憶行為,但是ERβ是否調(diào)控actin細(xì)胞骨架聚合尚不清楚。目的:探討ERβ在調(diào)控海馬神經(jīng)元actin細(xì)胞骨架多聚化以及學(xué)習(xí)記憶中的作用及其機(jī)制。方法:1、為了解ERβ在生后小鼠不同時(shí)相點(diǎn)海馬的表達(dá)情況,我們運(yùn)用蛋白質(zhì)免疫印跡(Western blot,WB)、免疫組化(Immunohistochemistry,IHC)實(shí)驗(yàn)方法檢測(cè)了ERβ在生后不同發(fā)育時(shí)期(P0,P7,P14,P28,P56)雌、雄小鼠海馬的表達(dá)變化。2、為了探討激活ERβ對(duì)海馬actin細(xì)胞骨架聚合以及學(xué)習(xí)記憶的影響,將成年小鼠進(jìn)行卵巢切除(ovariectomy,OVX),1w后在頸背部皮下注射不同劑量ERβ激動(dòng)劑DPN進(jìn)行預(yù)實(shí)驗(yàn),分為假手術(shù)對(duì)照(Control)、卵巢切除(OVX)、OVX+1.25 mg/kg DPN、OVX+2.5 mg/kg DPN、OVX+5.0 mg/kg DPN共5組,通過(guò)檢測(cè)上述處理?xiàng)l件下海馬SRC-1、Rictor及下游靶分子p-AKT以及actin細(xì)胞骨架聚合蛋白(p-cofilin/cofilin、Profilin-1)的表達(dá)變化確定DPN處理的最佳劑量。然后,在最佳劑量(5.0 mg/kg DPN)的處理?xiàng)l件下,檢測(cè)了DPN對(duì)OVX后上述分子表達(dá)、actin聚合狀態(tài)(F-actin/G-actin比值)的變化、海馬樹(shù)突棘密度以及學(xué)習(xí)記憶行為變化的調(diào)控。3、取成年動(dòng)情間期雌性小鼠,腹腔注射相同劑量(100ug/kg)ERβ抑制劑PHTPP,分為溶劑對(duì)照(Control)及PHTPP注射1、3、5、7d共5組,通過(guò)檢測(cè)海馬SRC-1、Rictor及下游靶分子p-AKT、p-cofilin/cofilin、Profilin-1的表達(dá)變化來(lái)確定PHTPP處理的最佳時(shí)間點(diǎn)。然后,在此最佳時(shí)間點(diǎn)(7d)條件下,運(yùn)用Morris水迷宮方法觀察小鼠空間記憶行為的變化情況,用WB、IHC以及高爾基鍍銀染色等方法來(lái)檢測(cè)抑制ERβ活性后海馬SRC-1、Rictor、p-AKT和actin細(xì)胞骨架聚合蛋白(p-cofilin/cofilin、Profilin-1)的表達(dá)變化、actin聚合狀態(tài)(F-actin/G-actin比值)、海馬區(qū)的樹(shù)突棘密度的變化,以此來(lái)探索ERβ活性改變與學(xué)習(xí)記憶之間的相互聯(lián)系。結(jié)果:1、ERβ在雌、雄小鼠P0、P7、P14、P28、P56海馬中都有表達(dá)。在P0時(shí)表達(dá)高,在P7和P14時(shí)表達(dá)下降,在P28和P56時(shí)表達(dá)增加。雄性小鼠在P28時(shí)達(dá)到P0時(shí)水平,但雌性小鼠在P28時(shí)就已高于P0時(shí)的表達(dá)。2、OVX后海馬SRC-1、Rictor及下游靶分子p-AKT、actin細(xì)胞骨架聚合蛋白(p-cofilin/cofilin、Profilin-1)表達(dá)均下降,1.25mg/kg DPN時(shí)僅Profilin-1的表達(dá)增加而其余分子表達(dá)無(wú)明顯變化,在2.5-5.0mg/kg DPN時(shí)上述所有分子表達(dá)較OVX組上升,因此,選取5.0mg/kg為DPN的最佳劑量。Morris水迷宮發(fā)現(xiàn)OVX后雌性小鼠的學(xué)習(xí)記憶下降,高爾基鍍銀染色結(jié)果顯示OVX組海馬樹(shù)突棘密度減少,免疫組織化學(xué)實(shí)驗(yàn)(immunohistochemistry,IHC)和蛋白印跡實(shí)驗(yàn)(Western blot,WB)顯示OVX組SRC-1、Rictor及下游靶分子p-AKT、actin細(xì)胞骨架聚合調(diào)控蛋白、actin聚合狀態(tài)(F-actin/G-actin比值)的表達(dá)下降,5.0mg/kg DPN處理可以逆轉(zhuǎn)OVX所致的上述變化。3、海馬SRC-1、Rictor、p-AKT、actin細(xì)胞骨架聚合調(diào)控蛋白(p-cofilin/cofilin、Profilin-1)在給予PHTPP注射5d時(shí)表達(dá)開(kāi)始下降,除Profilin-1外其余各分子表達(dá)在7d時(shí)顯著下降,因此,確定7d為PHTPP處理的最佳時(shí)間。在此條件下,Morris水迷宮發(fā)現(xiàn)PHTPP可致雌性小鼠的學(xué)習(xí)記憶下降,高爾基鍍銀染色結(jié)果顯示海馬樹(shù)突棘密度減少,IHC和Western blot顯示PHTPP下調(diào)海馬SRC-1、Rictor及下游靶分子p-AKT、actin細(xì)胞骨架聚合相關(guān)蛋白、actin聚合程度(F-actin/G-actin比值)的表達(dá)。結(jié)論:1、ERβ在雌、雄小鼠生后海馬內(nèi)(P0~P56)均有表達(dá),且在出生時(shí)和成年時(shí)維持在較高水平,呈現(xiàn)出“U-型”變化的趨勢(shì)。2、激活ERβ可逆轉(zhuǎn)OVX所致的海馬SRC-1、Rictor及下游靶分子p-AKT、actin細(xì)胞骨架聚合蛋白表達(dá)及海馬樹(shù)突棘密度的下降、actin聚合狀態(tài)的解聚和學(xué)習(xí)記憶行為障礙,提示活化ERβ可通過(guò)促進(jìn)actin細(xì)胞骨架的聚合進(jìn)而影響學(xué)習(xí)記憶行為。3、抑制ERβ可下調(diào)海馬SRC-1、Rictor及下游效應(yīng)分子p-AKT、actin細(xì)胞骨架聚合蛋白表達(dá)以及海馬樹(shù)突棘密度,促進(jìn)actin聚合狀態(tài)的解聚,動(dòng)物出現(xiàn)明顯的學(xué)習(xí)記憶行為障礙,提示抑制ERβ活性通過(guò)促進(jìn)actin細(xì)胞骨架的解聚進(jìn)而導(dǎo)致學(xué)習(xí)記憶行為障礙。綜上所述,在本研究中,采用了卵巢切除、Morris水迷宮、IHC、Western blot以及高爾基鍍銀染色等多種實(shí)驗(yàn)技術(shù),研究了調(diào)節(jié)ERβ活性變化對(duì)小鼠空間學(xué)習(xí)記憶行為以及SRC-1、m TORC2通路蛋白和actin細(xì)胞骨架聚合的影響,結(jié)合文獻(xiàn)我們認(rèn)為ERβ可能通過(guò)SRC-1/m TORC2調(diào)節(jié)actin細(xì)胞骨架聚合狀態(tài)的變化來(lái)影響突觸可塑性,最終對(duì)學(xué)習(xí)記憶行為產(chǎn)生影響。以上研究結(jié)果也為尋找AD預(yù)防和治療的新靶點(diǎn)提供了新的實(shí)驗(yàn)依據(jù)。
[Abstract]:It is reported that the decrease of estrogen (E_2), which is caused by aging, plays an important role in the learning and memory of Alzheimer's disease (Alzheimer 's disease, AD). The specific pathogenesis of AD is still not complete, and the therapeutic effect of the existing treatment is not ideal. Exploring the pathogenesis and treatment of AD has a profound influence on the prevention and treatment of AD, the promotion of medical care and family care, which not only affects the physiological development of women, but also plays an active role in improving the memory decline of the aged, and in regulating the plasticity of synaptic plasticity in the hippocampus and the regulation of learning and memory. The receptors that require the participation of estrogen receptor (ER) to produce.E_2 are divided into two categories: one is the membrane receptor GPR30, and the membranous components in the cell include the cell membrane, the mitochondrial membrane, the endoplasmic reticulum, and the second messenger pathway to mediate the regulation of some physiological functions by E_2; the other is the classic nuclear receptor, including the receptor. Estrogen receptor (estrogen receptor alpha, ER alpha) and estrogen beta receptor (estrogen receptor beta, ER beta), which mainly regulate the transcription of the target gene by binding to DNA in the nucleus. Steroid receptor auxiliary activating factor -1 (steroid receptor coactivator-1, SRC-1) is essential for promoting the nuclear receptor to regulate target gene transcription activities. One of the cofactors, highly expressed in the hippocampus, cerebral cortex, and other brain regions, its expression is affected by postpartum development and gonadectomy. Studies have shown that the expression of synaptic protein and the density of synapses and dendrites of the hippocampus are significantly decreased after the treatment of ovariectomy and the treatment of nuclear receptor inhibitors. Estrogen replacement therapy and its nuclear receptor agonists can be used. The expression of synaptic protein and the density of dendritic spines are increased, but the mechanism of the role of ER beta in the.ER beta is not yet clear in 1996. The last 20 years of research have found that ER beta has been widely expressed in various animal bodies, and is involved in the regulation of E_2 on various brain functions, and the expression distribution and function in different partitions. In the central nervous system, there are a large number of ER beta expressions in the cerebral cortex and hippocampus, suggesting that ER beta may play a role in the functional receptors that mediate the learning and memory of E_2. The presence of ER beta in the reproductive system, the testis and the ovary can be detected, and it may be involved in E_2 regulation of the growth of the germ cells. In addition, ER beta m RNA can also be detected in cardiovascular, digestive tract and other systems, and it also has a very important physiological significance. In the brain, it was found that the expression of synaptic protein in the hippocampus was significantly decreased, the density of dendritic spines decreased, and spatial learning was found by using ER beta specific antagonists and gene knockout methods to inhibit ER beta. The activation of ER beta through ER beta agonists can improve synaptic plasticity and improve spatial learning and memory, suggesting that ER beta has an important regulation on learning and memory, but its specific mechanism is not yet clear. Actin (actin) is an important component of the cytoskeleton, and the dynamic changes in actin polymerization and depolymerization are the basis of synaptic plasticity. It is the basis of learning and memory. Spherical actin (G-actin) is polymerized into a spiral actin (F-actin) under the induction of Profilin-1 and other molecules. Therefore, the change in the proportion of F-actin/G-actin is often used as a measure of the degree of actin polymerization. The study also found that the mammalian rapamycin target protein complex 2 (mammalian target) Of rapamycincomplex 2, m TORC2) plays an important role in the regulation of the aggregation of the cytoskeleton of the actin. The core component of the m TORC2, Rictor, leads to a decrease in the degree of actin polymerization and dendrite density, and the cause of serious learning and memory disorders. The effect molecule p-AKT (AKT) can reverse the impairment of learning and memory. M TORC2 plays an important role in regulating the cytoskeleton polymerization and learning memory of actin. Previous studies have reported that ER beta can regulate dendrite density and learning and memory behavior, but whether ER beta regulates the aggregation of actin cytoskeleton is unclear. Objective: To explore the role of ER beta in regulating the cytoskeleton polycondensation and learning memory of hippocampal neurons in actin. Methods: 1, in order to understand the expression of ER beta in the hippocampus of different phases of the mice after birth, we used Western blot (WB) and immunohistochemistry (Immunohistochemistry, IHC) to detect the expression of ER beta in the different developmental stages (P0, P7, P14, P28, P56) and the expression of the hippocampus in male mice, in order to explore the excitation of the hippocampus. The effects of ER beta on the cytoskeleton polymerization and learning and memory of hippocampal actin cells were treated with ovariectomy (OVX) in adult mice (ovariectomy, OVX). After 1W, different doses of ER beta agonist DPN were injected subcutaneously into the back of the neck to be pre tested, divided into the sham operation control (Control), the ovariectomy (OVX), OVX+1.25 mg/kg DPN, and 5 The optimal dosage of DPN treatment was determined by detecting the expression changes of the hippocampal SRC-1, Rictor, the downstream target molecule p-AKT and the actin cytoskeleton polymeric protein (p-cofilin/cofilin, Profilin-1) under the above treatment conditions. Then, under the best dose (5 mg/kg DPN), the expression of DPN to OVX was detected and actin polymerized. The changes in the state (F-actin/G-actin ratio), the density of the hippocampal dendrites and the changes in the learning and memory behavior were regulated by.3. The adult estrus female mice were intraperitoneally injected with the same dose (100ug/kg) ER beta inhibitor PHTPP, divided into 5 groups, solvent control (Control) and PHTPP injection 1,3,5,7d, by detecting the hippocampus SRC-1, Rictor and downstream target molecule p-AKT, p-. Cofilin/cofilin, Profilin-1 expression changes to determine the best time point for PHTPP treatment. Then, under the best time point (7D), the Morris water maze method was used to observe the changes in the spatial memory behavior of mice. WB, IHC, and Golgi silver staining were used to detect the hippocampus SRC-1, Rictor, p-AKT and acti after the inhibition of ER beta activity. The changes in the expression of N cytoskeleton poly (p-cofilin/cofilin, Profilin-1), actin polymerization state (F-actin/G-actin ratio) and the density of dendritic spines in the hippocampus in order to explore the relationship between the changes of ER beta activity and learning memory. Results: 1, ER beta is expressed in female, male mice P0, P7, P14, P28, P56 hippocampus. The expression decreased at P7 and P14, and increased at P28 and P56. The male mice reached the level of P0 at P28, but the female mice were higher than P0 when P28 was higher than P0. The hippocampus SRC-1, Rictor and downstream target molecules were decreased. The expression of IN-1 was increased and the expression of other molecules was not obviously changed. The expression of all the above molecules increased at 2.5-5.0mg/kg DPN. Therefore, the optimum dose of.Morris water maze of 5.0mg/kg as DPN was selected to find the decline of learning and memory in the female mice after OVX, and the Golgi Golgi staining fruit showed that the density of the dendritic spines in the hippocampus of the hippocampus was reduced in the OVX group and the immune group was in the immune group. Immunohistochemistry (IHC) and Western blot experiments (Western blot, WB) showed that OVX group SRC-1, Rictor, and downstream target molecules p-AKT, actin cytoskeleton polymerization regulatory proteins, actin polymerization state (F-actin/G-actin ratio) decreased. T, actin cytoskeleton polymerization regulatory protein (p-cofilin/cofilin, Profilin-1) began to decrease when given PHTPP injection of 5D, and the expression of other molecules except Profilin-1 was decreased significantly. Therefore, the optimal time for 7d to be treated as PHTPP was determined. Under this condition, the Morris water maze found that the learning and memory of PHTPP to female mice decreased. The result of silver plating staining showed that the density of hippocampal dendrites decreased, and IHC and Western blot showed that PHTPP lowered the SRC-1, Rictor and downstream target molecules p-AKT, actin cytoskeleton aggregation related proteins and actin polymerization degree (F-actin/G-actin ratio). Conclusion: 1, ER beta was expressed in the hippocampus (P0~P56) in male mice after birth and at birth. At the time and in adulthood, it is maintained at a high level, showing a "U- type" change trend.2. Activation of ER beta can reverse OVX induced SRC-1, Rictor and downstream target molecules p-AKT, actin cytoskeleton polymerization protein expression and the decrease of hippocampal dendrite density, actin polymerization state depolymerization and learning memory behavior disorder, suggesting that activation ER beta can be promoted by promoting the activation of ER beta. The aggregation of the actin cytoskeleton further affects the learning and memory behavior.3, and the inhibition of ER beta can downregulate the SRC-1, Rictor and downstream effector p-AKT, the expression of the actin cytoskeleton polymerized protein and the density of the hippocampal dendrite, which promotes the depolymerization of the actin polymerization state, and the animals have obvious learning memory behavior disorders, suggesting that the inhibition of ER beta activity is promoted through the promotion of promoting the activity of ER beta. The depolymerization of the cytoskeleton into actin leads to the learning and memory behavior disorder. In this study, in this study, a variety of experimental techniques, such as ovariectomy, Morris water maze, IHC, Western blot and Golgi Golgi staining, were used in this study to study the learning and memory behavior of ER beta activity and SRC-1, m TORC2 pathway protein and act. The effect of in cytoskeleton polymerization, combined with the literature, we think that ER beta may affect the synaptic plasticity by regulating the changes in the aggregation of the actin cytoskeleton through the SRC-1/m TORC2, and ultimately affects the learning and memory behavior. The results also provide new experimental evidence for the search for new targets for the prevention and treatment of AD.

【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R473.74

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