本文關(guān)鍵詞： 慢性應(yīng)激 抑郁癥 腦源性神經(jīng)營養(yǎng)因子 艾司西酞普蘭　出處：《東南大學(xué)》2015年碩士論文　論文類型：學(xué)位論文

【摘要】：目的：基于抑郁癥的神經(jīng)營養(yǎng)假說,本研究通過慢性不可預(yù)知溫和應(yīng)激(CUMS)制作抑郁癥大鼠模型,對抑郁癥大鼠予以艾司西酞普蘭抗抑郁劑干預(yù),觀察大鼠行為學(xué)變化,檢測腦脊液、血清腦源性神經(jīng)營養(yǎng)因子(BDNF)的變化,探討B(tài)DNF與抑郁癥的發(fā)病關(guān)系及艾司西酞普蘭干預(yù)對BDNF的影響。方法：采用CUMS制作抑郁癥大鼠模型,運用強迫游泳實驗(forced swimming test,FST)、蔗糖水偏愛實驗(sucrose preference test,SPT)、曠場實驗(open field test,OFT)和體重增長評估大鼠抑郁行為及艾司西酞普蘭抗抑郁劑干預(yù)后行為學(xué)變化,ELISA法檢測抑郁模型大鼠及艾司西酞普蘭干預(yù)后大鼠腦脊液、血清BDNF的含量。結(jié)果：1.建模4w時,與非應(yīng)激大鼠相比,應(yīng)激大鼠FST實驗中不動時間顯著延長[(15.18±8.39)s vs.(73.33±34.71)s],SPT實驗中蔗糖消耗百分比顯著降低[(86.21±5.54)%vs.(69.68±14.29)%],OFT實驗中總路程顯著縮短[(1328.65±513.29)cm Vs.(375.71±176.18)cm]、直立次數(shù)顯著減少[(19.58±6.90)次vs.(3.25±3.25)次],體重增長顯著減慢[(376.04±27.27)g vs.(318.97±34.290)g],差異均有統(tǒng)計學(xué)意義(p0.01)。2.藥物干預(yù)4w時,與抑郁模型組相比,抑郁給藥組FST實驗中不動時間顯著縮短[(59.50±31.06)s vs.(20.41±10.67)s],SPT實驗中蔗糖消耗百分比顯著增加[(48.81±18.90)%vs.(85.27±7.76)%],OFT實驗中總路程顯著增加[(267.76±255.56)cm vs.(1190.41±306.64)cm],差異均有統(tǒng)計學(xué)意義(p0.05)。OFT實驗中直立次數(shù)比較[(5.17±3.71)次vs.(11.17±1.33)次]、體重比較[(354.73±34.03)g vs.(338.43±40.67)g],差異均無統(tǒng)計學(xué)意義(p0.05)。3.藥物干預(yù)4w時,正常給藥組與正常對照組FST實驗中不動時間比較[(14.00±6.60)s vs.(18.39±5.37)s]、SPT實驗中蔗糖消耗百分比比較[(90.19±4.28)% vs.(94.08±2.66)%]、OFT實驗中總路程比較[(1575.06±471.96)cm vs.(1373.38±316.30)cm]、直立次數(shù)比較[(14.17±4.45)次vs.(17.67±1.67)次]、體重比較[(437.30±57.24)g vs.(417.03±43.82)g],差異均無統(tǒng)計學(xué)意義(p0.05)。4.腦脊液BDNF水平：與正常對照組相比,抑郁模型組CSFBDNF水平顯著降低[(1306.30±170.15)pg/ml vs.(1064.69±97.31)pg/ml]；與抑郁模型組相比,抑郁給藥組CSF BDNF水平顯著升高[(1064.69±97.31)pg/ml vs.(1320.36±189.23)pg/ml],差異均有統(tǒng)計學(xué)意義(p0.05)。與正常對照組相比,正常給藥組CSF BDNF水平無顯著變化[(1306.30±170.15)pg/ml vs.(1416.32±73.48)pg/ml],差異無統(tǒng)計學(xué)意義(p0.05)。5.血清BDNF水平：與正常對照組相比,抑郁模型組血清BDNF水平顯著降低[(688.14±68.87)pg/ml vs.(374.16±166.73)pg/ml]；與抑郁模型組相比,抑郁給藥組血清BDNF水平顯著升高[(374.16±166.73)pg/ml vs.(844.17±79.57)pg/ml],差異均有統(tǒng)計學(xué)意義(p0.01)。與正常對照組相比,正常給藥組血清BDNF水平無顯著變化[(688.14±68.87)pg/ml vs.(544.90±97.35)pg/ml],差異無統(tǒng)計學(xué)意義(p0.05)。結(jié)論：抑郁模型大鼠腦脊液、血清BDNF水平降低,艾司西酞普蘭干預(yù)能改善抑郁大鼠的抑郁行為,升高抑郁模型大鼠腦脊液、血清BDNF水平,而對正常大鼠無影響。
[Abstract]:Objective: the neurotrophic hypothesis of depression based on the research by chronic unpredictable mild stress (CUMS) model of depression rats to escitalopram depression rats of antidepressant intervention, behavioral changes of the rats were observed, cerebrospinal fluid, serum brain-derived neurotrophic factor (BDNF) changes of BDNF with the onset of depression and escitalopram intervention on BDNF. Methods: the rat model of depression by CUMS, using the forced swimming test (forced swimming, test, FST), sucrose preference test (sucrose preference, test, SPT), open field test (open field, test, OFT) and weight growth evaluation of depression the behavior of rats and the antidepressant escitalopram intervention behavior, detection of depression model rats and escitalopram intervention ELISA method after cerebral spinal fluid, the content of BDNF in serum. Results: 1. 寤烘ā4w鏃，

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