本文選題：老年性癡呆　切入點(diǎn)：同病異證　出處：《山西中醫(yī)學(xué)院》2016年碩士論文

【摘要】：目的:本課題以AD的兩個(gè)病證結(jié)合模型:病(老年性癡呆,簡(jiǎn)稱AD)加證(腎陽(yáng)虛、痰濁阻竅)為研究對(duì)象,以該病的六個(gè)主要發(fā)病機(jī)制,即Tau蛋白異常、淀粉樣前體蛋白代謝失調(diào)、膽堿能系統(tǒng)紊亂、神經(jīng)細(xì)胞凋亡、泛素-蛋白酶體通路(UPP)異常、免疫炎癥反應(yīng)等的相關(guān)系列指標(biāo):Tau蛋白、Aβ、Ach和Ach E、Bax和Bcl-2、Ub和E1、P65為研究?jī)?nèi)容,利用分子生物學(xué)技術(shù)手段,探索AD兩個(gè)典型證候的生物學(xué)內(nèi)涵,尋找AD“同病異證”在生物學(xué)機(jī)制方面的共性及特異性。方法:將13只6月齡SAMR1小鼠分為正常組,39只6月齡SAMP8小鼠隨機(jī)平均分為3組,每組13只,分別為AD模型組(簡(jiǎn)稱模型組)、腎陽(yáng)虛證AD模型組(簡(jiǎn)稱腎虛組)、痰濁阻竅證AD模型組(簡(jiǎn)稱痰濁組)。腎虛組采用腹腔內(nèi)注射氫化可的松的方法復(fù)制腎陽(yáng)虛證AD模型;痰濁組采用飼喂6W高脂飼料的方法復(fù)制痰濁阻竅證AD模型。模型復(fù)制成功后,采集所需標(biāo)本,分別從光鏡(肝臟和腎臟組織)、電鏡(海馬)、生化指標(biāo)(血液、海馬和大腦皮層)等不同層面,尋找AD腎陽(yáng)虛證與痰濁阻竅證在生物學(xué)機(jī)制方面的共性與特異性。結(jié)果:1.形態(tài)學(xué)結(jié)果小鼠肝臟、腎臟光鏡及海馬電鏡結(jié)果顯示,正常組小鼠的肝臟、腎臟及海馬組織超微結(jié)構(gòu)未見(jiàn)明顯異常;模型組小鼠的肝臟、腎臟及海馬組織超微結(jié)構(gòu)有輕度損害;痰濁組小鼠各組織的損害較正常組略重,腎虛組小鼠各組織的損害最重。2.海馬、大腦皮層和血液生化指標(biāo)檢測(cè)結(jié)果2.1模型組與正常組比較:兩組小鼠大腦皮層中Tau蛋白、Aβ和海馬中Bax含量有顯著性差異(P0.05),模型組Tau蛋白、Aβ、Bax含量較正常組高。兩組小鼠在大腦皮層中Ach和AchE以及海馬中Bcl-2、Ub和E1、P65指標(biāo)方面均無(wú)顯著性差異。2.2腎虛組與正常組比較:兩組小鼠血液中ACTH和CORT含量均有顯著性差異(P0.05),腎虛組小鼠ACTH和CORT含量較正常組低。2.3痰濁組與正常組比較:兩組小鼠血液中TG含量有顯著性差異(P0.05),痰濁組TG含量較正常組高,且為正常組TG含量的1.56倍。2.4腎虛組與痰濁組比較:腎虛組小鼠大腦皮層中Tau蛋白、Aβ和海馬中Bax含量較痰濁組高,海馬中Bcl-2含量較痰濁組低,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。兩組小鼠大腦皮層中Ach和AchE及海馬中Ub和E1、P65含量無(wú)統(tǒng)計(jì)學(xué)差異。結(jié)論:腎陽(yáng)虛證與痰濁阻竅證時(shí)AD的以下三個(gè)機(jī)制,即Tau蛋白異常、淀粉樣前體蛋白代謝失調(diào)和神經(jīng)細(xì)胞凋亡會(huì)有明顯的異常,腎陽(yáng)虛證時(shí)此三種機(jī)制的異常較痰濁阻竅證時(shí)更明顯,腎陽(yáng)虛證時(shí)AD小鼠大腦的損害較痰濁阻竅證時(shí)的損害表現(xiàn)更突出。
[Abstract]:Objective: in this study, two models of AD combined with syndromes: disease (AD) plus syndrome (kidney-yang deficiency, phlegm-turbid obstruction of orifices) were used to study the six main pathogenesis of AD, that is, abnormal Tau protein.Amyloid precursor protein metabolism disorder, cholinergic system disorder, neuronal apoptosis, UPP abnormality of ubiquitin proteasome pathway, immune inflammatory response, and other related indexes, such as A 尾 -Ach, Ach eau Bax, Bcl-2Ub and E1P65, were studied.By means of molecular biology technique, the biological connotation of two typical symptoms of AD was explored, and the commonness and specificity of the biological mechanism of AD "same disease and different syndrome" were found.Methods: thirteen 6-month-old SAMR1 mice were divided into normal group (n = 39) and 6-month-old SAMP8 mice (n = 39).AD model group (abbreviated as model group), kidney yang deficiency syndrome AD model group (abbreviated as kidney deficiency group), phlegm turbid obstruction syndrome AD model group (abbreviated phlegm turbid group).The AD model of kidney-yang deficiency syndrome was induced by intraperitoneal injection of hydrocortisone in kidney-deficiency group, and the AD model of phlegm-turbid obstruction syndrome was induced by feeding 6W high-fat diet in phlegm-turbid group.After the model was successfully duplicated, samples were collected from different levels, such as light microscope (liver and kidney tissue, electron microscope (hippocampus), biochemical indexes (blood, hippocampus and cerebral cortex), etc.To find the commonness and specificity of AD kidney yang deficiency syndrome and phlegm turbid obstruction syndrome in biological mechanism.The result is 1: 1.The ultrastructure of liver, kidney and hippocampal tissue in normal group was not abnormal, while in model group there was slight damage in liver, kidney and hippocampal tissue.The damage of each tissue in phlegm turbid group was slightly more serious than that in normal group, and that in kidney deficiency group was the most serious. 2.Results the biochemical indexes of hippocampus, cerebral cortex and blood in the model group were compared with those in the normal group: there was a significant difference in the contents of Tau protein A 尾 and Bax in hippocampus between the two groups. The content of Tau protein A 尾 -Bax in the model group was higher than that in the normal group.Compared with the normal group, the content of CORT in the blood of the group with phlegm turbidity was significantly higher than that in the group of phlegm turbidity (P 0.05), and the content of TG in the group of phlegm turbidity was higher than that in the group of normal phlegm.Compared with phlegm turbid group, the content of Tau protein A 尾 in cerebral cortex and Bax in hippocampus in kidney deficiency group were higher than those in phlegm turbid group, and Bcl-2 content in hippocampus was lower than that in phlegm turbid group (P 0.05).There was no significant difference in the contents of Ach and AchE in cerebral cortex and Ub and E1p65 in hippocampus between the two groups.Conclusion: there are three mechanisms of AD in the syndrome of kidney-yang deficiency and phlegm-turbid obstruction of orifices, that is, abnormal Tau protein, abnormal metabolism of amyloid precursor protein and apoptosis of nerve cells.The abnormality of these three mechanisms in kidney yang deficiency syndrome was more obvious than that in phlegm turbid obstruction of orifices syndrome. The brain damage of AD mice with kidney yang deficiency syndrome was more prominent than that of phlegm turbid orifices syndrome.
【學(xué)位授予單位】：山西中醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：R277.7

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