本文選題：創(chuàng)傷性腦損傷 + 腦外傷后抑郁　； 參考：《第三軍醫(yī)大學(xué)》2015年博士論文

【摘要】：背景:創(chuàng)傷性顱腦損傷(Traumatic brain injury,TBI)于全球范圍內(nèi)都是45歲以下年輕人群首要致死和致殘病因,TBI后最容易被臨床醫(yī)生所忽視的是精神情感障礙。外傷后抑郁(Post-trauma Depression)作為腦外傷后最常見(jiàn)的神經(jīng)精神后遺癥,目前發(fā)生機(jī)制尚不明確,也沒(méi)有療效明確的治療手段。在獎(jiǎng)勵(lì)機(jī)制、認(rèn)知、喚醒等方面發(fā)揮著重要作用的多巴胺(Dopamine,DA)被認(rèn)為在抑郁癥的發(fā)生過(guò)程中扮演著關(guān)鍵角色。TBI所造成的繼發(fā)性腦損傷可能破壞黑質(zhì)-紋狀體通路(Nigrostriatial Pathway),阻礙多巴胺能神經(jīng)元轉(zhuǎn)運(yùn)分泌的功能,從而影響中樞神經(jīng)系統(tǒng)多巴胺系統(tǒng)的功能。我們推斷TBI后抑郁的發(fā)生和腦內(nèi)黑質(zhì)-紋狀體通路穩(wěn)態(tài)的破壞密切相關(guān)。金剛烷胺,作為臨床上應(yīng)用于帕金森病(Parkinson’s disease,PD)的藥物,具有增加多巴胺生成和抑制多巴胺重?cái)z取的作用。近年來(lái),金剛烷胺應(yīng)用于TBI后意識(shí)、認(rèn)知、運(yùn)動(dòng)等功能恢復(fù)中的作用引起了學(xué)術(shù)界的廣泛關(guān)注。上述證據(jù)提示金剛烷胺可能成為TBI后有效的抗抑郁藥物。腦出血(intracerebral hemorrhage,ICH)作為死殘率極高的突發(fā)性疾病,迄今尚無(wú)有效的干預(yù)策略和治療手段。ICH造成的局部血腫不僅可以對(duì)出血周圍腦組織造成直接的應(yīng)力壓迫效應(yīng),而且在數(shù)小時(shí)到數(shù)天內(nèi)引發(fā)繼發(fā)性腦損傷(secondary brain injury)。大量的證據(jù)顯示繼發(fā)性腦損傷可能造成遲發(fā)性神經(jīng)功能缺損(delayed neurological deficit),血腦屏障(Blood Brain Barrier,BBB)的破壞及白質(zhì)纖維束的斷裂,而針對(duì)繼發(fā)性腦損傷的治療是有一定的治療時(shí)間窗。目前探索針對(duì)早期腦損傷(early brain injury,EBI)有保護(hù)作用的治療手段顯得格外的關(guān)鍵。亞低溫治療作為一種綜合治療手段,已經(jīng)用于多項(xiàng)臨床轉(zhuǎn)化。但最近三項(xiàng)關(guān)于物理性亞低溫治療腦外傷的多中心隨機(jī)臨床試驗(yàn)結(jié)果都宣告失敗,這可能和物理降溫屬于外源性體溫調(diào)節(jié)導(dǎo)致的寒顫引發(fā)應(yīng)激反應(yīng),激活交感神經(jīng),釋放兒茶酚胺,減少局部腦供血量相關(guān)。8-OH-DPAT,藥理作用和選擇性五羥色胺再攝取抑制劑類抗抑郁藥物(Selective Serotonin Reuptake Inhibitor,SSRI)所類似,神經(jīng)保護(hù)作用逐漸被研究者們所認(rèn)識(shí)�；瘜W(xué)性降溫作用于內(nèi)源性體溫調(diào)整系統(tǒng),直接作用于下丘腦視前區(qū)-下丘腦前部(preopticanteriorhypothalamus,po/ah),較物理性降溫的降溫過(guò)程更符合生理過(guò)程。第一部分腦外傷后抑郁發(fā)生機(jī)制及干預(yù)目的:研究腦外傷后腦內(nèi)多巴胺水平對(duì)外傷后抑郁發(fā)生的影響,并探究金剛烷胺對(duì)外傷后抑郁樣行為的治療效果材料和方法:1、健康成年雄性sd大鼠296只,隨機(jī)分為4組:假手術(shù)組、tbi組、金剛烷胺低劑量治療組和金剛烷胺高劑量治療組。治療組術(shù)后1小時(shí)第1次腹腔注射,之后每8小時(shí)給藥1次,高劑量組每日注射金剛烷胺135mg/kg,低劑量組每日注射45mg/kg,sham組和tbi組動(dòng)物予以等量生理鹽水作為對(duì)照。2、tbi后7d,14d,28d完成頭顱磁共振成像,觀察動(dòng)物腦挫傷程度。3、tbi后3d,7d,14d,28d進(jìn)行行為學(xué)實(shí)驗(yàn)(蔗糖攝取,曠場(chǎng)試驗(yàn),強(qiáng)迫游泳),評(píng)估動(dòng)物tbi后抑郁樣行為。4、4%多聚甲醛灌注后取腦組織,固定脫水后,完成he染色,fluoro-jadec染色觀察tbi后神經(jīng)元形態(tài)。5、westernblot法定量檢測(cè)tbi后中腦黑質(zhì)區(qū)tyrosinehydroxylase(th)活性。6、免疫熒光技術(shù)觀察中腦黑質(zhì)區(qū)多巴胺能神經(jīng)元tbi后凋亡。7、高效液相色譜-電化學(xué)法檢測(cè)tbi后3h,6h,12h,24h,3d,7d,14d,28d傷側(cè)大腦紋狀體多巴胺及其代謝產(chǎn)物(dopac和hva)含量。結(jié)果:1、tbi后7d,14d,28d,tbi組、tbi+a45組和tbi+a135組各組組間動(dòng)物腦挫傷體積無(wú)明顯差異。2、與sham組相比,tbi組于傷后3d,7d,14d,28d抑郁樣行為顯著增加,而金剛烷胺治療有效地改善了各個(gè)時(shí)間點(diǎn)動(dòng)物呈現(xiàn)出的抑郁樣行為。3、he染色顯示tbi7d各組紋狀體病理形態(tài)無(wú)明顯差異。fjc染色顯示手術(shù)后7d,tbi組紋狀體和中腦黑質(zhì)神經(jīng)元大量變性,而金剛烷胺治療有效地減少了中腦黑質(zhì)神經(jīng)元變性但對(duì)紋狀體神經(jīng)元變性無(wú)顯著性治療效果。4、westernblot結(jié)果提示:tbi組較sham組動(dòng)物中腦黑質(zhì)區(qū)th表達(dá)量明顯下調(diào)(p0.05),金剛烷胺治療有效地逆轉(zhuǎn)了th的下調(diào)趨勢(shì)。5、中腦黑質(zhì)區(qū)免疫熒光染色顯示:tbi組大量的多巴胺能神經(jīng)元發(fā)生凋亡,而金剛烷胺治療組多巴胺神經(jīng)元凋亡被有效的抑制了。6、tbi后各個(gè)時(shí)間點(diǎn)大腦紋狀體經(jīng)高效液相色譜-電化學(xué)法測(cè)定多巴胺及其代謝產(chǎn)物(dopac和hva)提示:tbi后3h,多巴胺能神經(jīng)遞質(zhì)有一過(guò)性的升高,而在亞急性期及慢性期都呈現(xiàn)持續(xù)性下降趨勢(shì),只在14d有過(guò)反彈性的增高。慢性金剛烷胺的治療可以有效地逆轉(zhuǎn)這種下降趨勢(shì)。結(jié)論:1、實(shí)驗(yàn)性tbi動(dòng)物在傷后不同時(shí)間點(diǎn)呈現(xiàn)出不同程度的抑郁樣行為,金剛烷胺治療有效地改善了tbi所致的抑郁樣行為。2、tbi后直接作用的紋狀體區(qū),he染色顯示:大量的神經(jīng)元壞死,細(xì)胞間水腫明顯,fjc染色證明大范圍地出現(xiàn)神經(jīng)元變性。金剛烷胺治療組紋狀體病理形態(tài)和tbi組無(wú)顯著性差異。3、tbi后,動(dòng)物中腦黑質(zhì)區(qū)多巴胺能神經(jīng)元變性凋亡明顯,同時(shí)中腦黑質(zhì)th活性明顯下調(diào)。予以金剛烷胺治療后,中腦黑質(zhì)變性及凋亡的多巴胺能神經(jīng)元明顯減少,th的活性顯著上調(diào)。4、高效液相色譜-電化學(xué)法結(jié)果顯示:tbi動(dòng)物紋狀體內(nèi)多巴胺及其代謝產(chǎn)物含量呈下降趨勢(shì),而金剛烷胺治療可以逆轉(zhuǎn)tbi后紋狀體多巴胺水平的降低。第二部分化學(xué)降溫劑對(duì)腦出血早期腦保護(hù)研究目的:本課題旨在8-oh-dpat發(fā)揮的降溫作用對(duì)ich后ebi及bbb的破壞是否具有保護(hù)作用,并比較化學(xué)性降溫劑和物理性亞低溫治療對(duì)ich動(dòng)物的腦保護(hù)效果。材料和方法:1、健康成年雄性sd大鼠207只,隨機(jī)分為假手術(shù)組(sham)、腦出血組(ich)、8-oh-dpat治療組(dpat)、物理性亞低溫治療組(hypo)。dpat組術(shù)后6小時(shí)完成第1次腹腔給藥,之后每天腹腔注射8-oh-dpat(1mg/kg)。hypo組于術(shù)后6小時(shí)開(kāi)始亞低溫治療,每日治療12小時(shí)。sham組和ich組動(dòng)物予以等量生理鹽水作為對(duì)照。2、ich后24h,72h進(jìn)行神經(jīng)功能評(píng)分和轉(zhuǎn)桿試驗(yàn),觀察運(yùn)動(dòng)功能缺損。3、傷后7d進(jìn)行morris水迷宮試驗(yàn),評(píng)估動(dòng)物ich后學(xué)習(xí)記憶能力。4、ich后6h,12h,24h,72h分別測(cè)量核心體溫和顱腦體表溫度。5、術(shù)后72h電鏡觀察海馬區(qū)神經(jīng)元亞顯微形態(tài)和結(jié)構(gòu)。6、ICH后24h,72h分別測(cè)量動(dòng)物腦水含量及BBB通透性。7、ICH后72h,應(yīng)用Western Blot法檢測(cè)出血灶周圍IL-1β及TNF-α表達(dá)量。結(jié)果:1、大鼠ICH模型可在早期造成神經(jīng)功能和學(xué)習(xí)記憶障礙,伴隨腦溫局部性升高。2、自體血注射模型引起顯著的急性腦水腫和BBB破壞,伴隨海馬神經(jīng)元大量變性壞死,出血周圍炎癥因子表達(dá)增加。3、物理性亞低溫治療一定程度上改善了ICH造成的神經(jīng)功能和學(xué)習(xí)記憶能力缺損,保護(hù)海馬區(qū)神經(jīng)細(xì)胞免于變性壞死,但對(duì)ICH造成的早期BBB破壞的保護(hù)效果不明確。4、8-OH-DPAT治療對(duì)ICH后腦溫升高的調(diào)節(jié)過(guò)程平緩且持續(xù),可以有效地減輕ICH后動(dòng)物神經(jīng)功能和學(xué)習(xí)記憶能力的損傷,保護(hù)了ICH造成的BBB通透性增加,減少了血腫周圍炎癥因子的表達(dá)。結(jié)論:1、大鼠ICH模型在損傷早期可造成腦溫升高,同時(shí)引起神經(jīng)功能缺損和學(xué)習(xí)記憶能力降低,伴隨BBB的破壞和海馬區(qū)神經(jīng)元壞死,提示腦溫異常可以是早期腦損傷的重要機(jī)制。2、化學(xué)性降溫劑8-OH-DPAT在ICH早期的腦保護(hù)作用優(yōu)于物理性亞低溫治療,可以有效地保護(hù)BBB的損傷,減少神經(jīng)元的變性壞死,減輕腦水腫發(fā)生,改善動(dòng)物ICH后神經(jīng)功能和學(xué)習(xí)記憶能力的缺損,說(shuō)明直接作用于體溫調(diào)節(jié)中樞的溫度干預(yù)可能成為中樞神經(jīng)系統(tǒng)損傷的一個(gè)新的治療靶點(diǎn)。
[Abstract]:Background: Traumatic brain injury (TBI) is the leading cause of death and disability of young people under 45 years of age. After TBI, the most likely to be neglected by clinicians is the mental and emotional disorder. Post traumatic depression (Post-trauma Depression) is the most common neuropsychiatric sequelae after brain trauma, and is currently occurring at present. The mechanism is not clear, and there is no effective treatment. Dopamine (DA), which plays an important role in the reward mechanism, cognition, and arousal, is considered to be a key role of.TBI in the process of depression. The secondary brain injury may break the substantia nigra striatum pathway (Nigrostriatial Pathway), and prevent it. The functions of dopaminergic neurons transport and secrete and affect the function of the dopamine system in the central nervous system. We infer that the occurrence of depression after TBI is closely related to the destruction of the homeostasis of the substantia nigra striatal pathway in the brain. Amantadine, a drug that is used clinically in Parkinson's disease (Parkinson 's disease, PD), has an increase in dopamine production. In recent years, the role of amantadine in TBI, cognitive, exercise and other functional recovery has attracted extensive attention in the academic world. The above evidence suggests that amantadine may become an effective antidepressant after TBI. Intracerebral hemorrhage (ICH) is a very high death rate. The local hematoma caused by.ICH, which has so far no effective intervention strategy and treatment, can not only cause direct stress stress on the brain tissue around the hemorrhage, but also cause secondary brain damage (secondary brain injury) within several hours to several days. A large number of evidence shows that secondary brain injury may cause late onset deity. After functional defect (delayed neurological deficit), the destruction of the blood brain barrier (Blood Brain Barrier, BBB) and the fracture of the white matter fiber bundle, there is a certain time window for the treatment of secondary brain injury. At present, the treatment of the early brain injury (early brain injury, EBI) is the key to the treatment of the secondary brain injury (early brain injury, EBI). As a comprehensive treatment, hypothermia therapy has been used for multiple clinical transformations, but the recent three multicenter randomized clinical trials of physical hypothermia treatment have failed, which may be associated with physical hypothermia due to exogenous thermoregulation induced stress response, activation of sympathetic nerve, and catechol release. Amines, reducing local brain blood supply related.8-OH-DPAT, pharmacological action and selective antidepressant (Selective Serotonin Reuptake Inhibitor, SSRI) of the selective five hydroxytryptamine reuptake inhibitor (Reuptake Inhibitor, SSRI), the neuroprotective effect is gradually recognized by the researchers. Chemical hypothermia acts on the endogenous hypothalamus, directly acting on the hypothalamus The preoptic region of the anterior hypothalamus (preopticanteriorhypothalamus, po/ah) is more suitable for physiological processes than physical cooling. Part 1: the mechanism and intervention of post traumatic depression: the study of dopamine levels in the brain after traumatic brain injury and the effect of amantadine on posttraumatic depression like behavior Treatment effect materials and methods: 1, 296 healthy adult male SD rats were randomly divided into 4 groups: sham operation group, TBI group, low dose amantadine treatment group and high dose amantadine treatment group. The treatment group was injected 1 hours and first times after operation, then 1 times every 8 hours, high dose group daily injection of amantadine 135mg/kg, low dose group daily injection. 45mg/kg, group sham and group TBI were given equal amount of normal saline as control.2, 7d, 14d, and 28d completed head magnetic resonance imaging after TBI, and observed the degree.3 of brain contusion in animals, 3D, 7d, and 7d. After dehydration, he staining was completed, fluoro-jadec staining was used to observe neuronal morphology after TBI, and Westernblot method was used to detect Tyrosinehydroxylase (th) active.6 in the mesencephalic substantia nigra after TBI, and the apoptosis of dopaminergic neurons in the mesencephalic substantia nigra region was observed by immunofluorescence technique. The content of dopamine and its metabolites (DOPAC and HVA) in the cerebral striatum of 28d. Results: 1, TBI after TBI, 7d, 14d, 28d, TBI, tbi+a45 group and tbi+a135 group, there was no significant difference in the volume of brain contusion between the groups of tbi+a45 and tbi+a135 groups. .3, he staining showed no significant difference in the pathomorphology of the striatum in tbi7d, and.Fjc staining showed that the striatum and the substantia nigra neurons in group TBI were significantly denatured after the operation, while amantadine therapy effectively reduced the degeneration of the substantia nigra neurons in the middle brain but had no significant treatment for the degeneration of the striatum neurons. The results of therapeutic effect.4, Westernblot results showed that the TH expression of th in group TBI was significantly lower than that in group sham (P0.05), and amantadine therapy effectively reversed the downward trend.5 of th. The immunofluorescence staining in the medium brain substantia nigra region showed that a large number of dopaminergic neurons in the group TBI were apoptotic, and the apoptosis of dopamine neurons in the amantadine group was also apoptotic. The.6 was effectively suppressed. After TBI, the brain striatum measured dopamine and its metabolites (DOPAC and HVA) by high performance liquid chromatography electrochemistry (DOPAC and HVA). After TBI 3h, the dopaminergic neurotransmitter had an excessive increase in the dopaminergic neurotransmitter, while both in the subacute and chronic stages showed a persistent downward trend, only in 14d with a higher anti elasticity. The treatment of chronic amantadine can effectively reverse this downward trend. Conclusion: 1, experimental TBI animals present different degrees of depressive behavior at different time points after injury. Amantadine therapy effectively improves the depressive behavior caused by TBI,.2, the striatum, which is directly affected by TBI, and he staining shows that a large number of neurons are necrotic. The intercellular edema was obvious, and FJC staining showed that the neuron degeneration appeared in a large range. There was no significant difference between the pathological morphology of the striatum and the TBI group in the treatment group of amantadine.3. After TBI, the degeneration of dopaminergic neurons in the substantia nigra area of the animal was obvious, and the activity of th in the middle cerebral substantia nigra was significantly lower. The apoptosis of dopaminergic neurons significantly decreased, the activity of th increased significantly by.4. The results of high performance liquid chromatography electrochemistry showed that the content of dopamine and its metabolites in the striatum of TBI animals decreased, while amantadine could reverse the decrease in the level of dopamine in the striatum after TBI. The second part of the chemical cooling agent was early on the brain hemorrhage. Objective: the purpose of this study is to investigate whether the cooling effect of 8-OH-DPAT plays a protective role on the destruction of EBI and BBB after ICH, and compares the protective effects of chemical cooling agents and physical hypothermia on ICH animals. Materials and methods: 1, 207 healthy adult male SD rats were randomly divided into sham operation group (sham) and cerebral hemorrhage. Group (ICH), 8-OH-DPAT treatment group (DPAT), physical hypothermia treatment group (hypo) group.Dpat after 6 hours to complete first times of intraperitoneal administration, then daily intraperitoneal injection of 8-OH-DPAT (1mg/kg).Hypo group at 6 hours to begin mild hypothermia treatment, 12 hours of daily treatment of.Sham group and ICH group of normal saline as a control.2, ICH after, proceed into the ICH .3 and 7d maze test after injury were performed to evaluate the learning and memory ability of animals after ICH and.4, 6h, 12h, 24h, 72h after ICH, respectively, to measure the temperature of the core and the temperature of the body surface in the brain after ICH, and the submicroscopic morphology and structure of the neurons in the hippocampus were observed after the operation. The brain water content, BBB permeability.7 and 72h after ICH were used to detect the expression of IL-1 beta and TNF- alpha around the hemorrhagic foci by Western Blot. Results: 1, the rat ICH model could cause neurological function and learning memory impairment in the early stage, with the brain temperature local increase.2, the autologous blood injection model led to significant acute cerebral edema and BBB destruction, accompanied by hippocampus God. After massive degeneration and necrosis, the expression of inflammatory factors around the hemorrhage increased.3. Physical hypothermia treatment improved the neural function and learning memory impairment caused by ICH to some extent and protected the hippocampal neurons from degeneration and necrosis, but the protective effect of the early BBB damage caused by ICH was not clear on the.4,8-OH-DPAT treatment of the ICH brain. The adjustment process of temperature rise is slow and continuous. It can effectively reduce the damage of nerve function and learning and memory ability after ICH, protect the increase of BBB permeability caused by ICH and reduce the expression of inflammatory factors around hematoma conclusion: 1, the rat ICH model can make the brain temperature rise at the early stage of injury and cause nerve function defect and learning at the same time. The decrease of memory ability, the destruction of BBB and the necrosis of neurons in the hippocampus suggest that abnormal brain temperature can be an important mechanism of early brain injury,.2. The protective effect of chemical cooling agent 8-OH-DPAT in early ICH is better than that of physical hypothermia. It can effectively protect the injury of BBB, reduce the degeneration and necrosis of neurons and reduce the occurrence of brain edema. To improve the impairment of neural function and learning and memory ability after ICH, it is suggested that the temperature intervention directly acting on the center of thermoregulation may be a new therapeutic target for the injury of central nervous system.

【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2015
【分類號(hào)】：R651.15

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