本文選題：腦卒中后抑郁 + 額前皮質(zhì)��； 參考：《神經(jīng)解剖學(xué)雜志》2017年06期

【摘要】：目的:探討腦卒中后抑郁(post-stroke depression,PSD)大鼠額前皮質(zhì)小膠質(zhì)細(xì)胞表達(dá)腦源性神經(jīng)營養(yǎng)因子(BDNF)及其高親和力受體酪氨酸激酶受體B(TrkB)的情況,了解小膠質(zhì)細(xì)胞在PSD發(fā)病機制中的作用。方法:將健康成年SD大鼠隨機分為正常組、抑郁組、腦卒中組和PSD組,每組10只。卒中組采用線栓法建立局灶性腦缺血模型;抑郁組采用慢性不可預(yù)見的中等應(yīng)激刺激(CUMS)結(jié)合孤養(yǎng)法建立大鼠慢性應(yīng)激抑郁模型;PSD組采用線栓法建立局灶性腦缺血模型后,再加以CUMS及孤養(yǎng)法建立PSD大鼠模型。于造模后第29 d(4周后)及第57 d(8周后)應(yīng)用免疫熒光雙標(biāo)染色法檢測各組大鼠額前皮質(zhì)小膠質(zhì)細(xì)胞表達(dá)BDNF及其高親和力受體TrkB的情況。結(jié)果:造模后第29 d PSD組額前皮質(zhì)OX42(小膠質(zhì)細(xì)胞標(biāo)記物)與BDNF免疫熒光雙標(biāo)陽性細(xì)胞及與TrkB免疫熒光雙標(biāo)陽性細(xì)胞平均光密度值均最小,正常對照組均最大。單因素方差分析結(jié)果顯示:PSD組與各對照組(抑郁組、腦卒中組、正常組)相比,差異均有統(tǒng)計學(xué)意義(P0.05);抑郁組及腦卒中組均較正常對照組小(P0.05)。造模后第57 d PSD組額前皮質(zhì)OX42與BDNF免疫熒光雙標(biāo)陽性細(xì)胞及OX42與TrkB免疫熒光雙標(biāo)陽性細(xì)胞平均光密度值均為最小,正常對照組均最大。PSD組與各對照組(抑郁組、腦卒中組、正常組)相比,差異均有統(tǒng)計學(xué)意義(P0.05);抑郁組也較正常對照組小(P0.05);腦卒中組也較正常對照組小(P0.05);抑郁組與腦卒中組相比,差異無統(tǒng)計學(xué)意義(P0.05)。結(jié)論:PSD大鼠額前皮質(zhì)小膠質(zhì)細(xì)胞表達(dá)BDNF及TrkB,其平均光密度值在PSD急性期及慢性期均明顯減少,可能與PSD發(fā)病機制相關(guān)。小膠質(zhì)細(xì)胞可能通過減少BDNF及其高親和力受體TrkB的表達(dá)在PSD發(fā)病過程中發(fā)揮了重要的作用。
[Abstract]:Aim: to investigate the expression of brain-derived neurotrophic factor (BDNF) and its high affinity receptor tyrosine kinase B (TrkB) in prefrontal cortex microglia of post-stroke depression- PSD rats, and to investigate the role of microglia in the pathogenesis of post-stroke. Methods: healthy adult SD rats were randomly divided into normal group, depression group, stroke group and PSD group with 10 rats in each group. In stroke group, focal cerebral ischemia model was established by thread occlusion, and chronic unpredictable moderate stress stimulation (CUMS) combined with solitary therapy was used to establish chronic stress depression model in depression group and focal cerebral ischemia model was established in PSD group with thread occlusion method. Then the rat model of PSD was established by CUMS and the method of solitary nourishment. The expression of BDNF and its high affinity receptor TrkB in prefrontal cortex microglia of rats in each group were detected by immunofluorescence double labeling method on the 29th (4 weeks) and 57 (8 weeks) after modeling. Results: the average optical density of prefrontal cortex OX42 (microglial cell marker) and BDNF double labeled positive cells and TrkB immunofluorescence positive cells were the lowest in PSD group on the 29th day after modeling, and were the largest in normal control group. The univariate ANOVA results showed that there were significant differences between the two groups (P 0.05); the depression group and stroke group were smaller than the normal control group (P0.05). The mean optical density of OX42 and BDNF double labeled positive cells and OX42 and TrkB immunofluorescence positive cells in prefrontal cortex of PSD group was the smallest on the 57th day after modeling, and the maximum optical density of OX42 and BDNF double labeled positive cells in PSD group was the highest in the normal control group and every control group (depression group, stroke group). Compared with the normal group, the difference was statistically significant (P0.05); the depression group was also smaller than the normal control group (P0.05); the stroke group was also smaller than the normal control group (P0.05); the depression group and the stroke group, the difference was not statistically significant (P0.05). Conclusion the expression of BDNF and TrkB in microglia of prefrontal cortex of the rats with PSD was significantly decreased in the acute and chronic phase of PSD, which may be related to the pathogenesis of PSD. Microglia may play an important role in the pathogenesis of PSD by reducing the expression of BDNF and its high affinity receptor TrkB.
【作者單位】： 大理大學(xué)臨床醫(yī)學(xué)院;大理大學(xué)第一附屬醫(yī)院神經(jīng)內(nèi)科;
【基金】：國家自然科學(xué)基金(81360208)
【分類號】：R743.3
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本文編號：2088890