电针对慢性应激抑制模型大鼠脑单胺类神经递质的影响

目的 探讨电针刺百会,印堂穴对慢性应激抑郁模型大鼠脑内单胺类神经递质的影响及治疗抑郁症的机理。方法 将２４只Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ雄性大鼠随机分为对照组,抑郁模型组,抑制模型电针组和抑郁模型加阿米替林组,每组６只,用高效液相－电化学法测定大鼠脑内单胺类神经递质及其代谢产物的含量,比较含量的比值。结果 抑郁模型组大鼠脑皮层５－羟色胺（５－ＨＴ）／５－羟吲哚乙酸（５－ＨＩＡＡ）,纹状体多巴胺（Ｄ     

电针对慢性应激抑郁模型大鼠脑单胺类神经递质的影响

目的　探讨电针刺激百会、印堂穴对慢性应激抑郁模型大鼠脑内单胺类神经递质的影响及治疗抑郁症的机理。方法　将２４ 只ＳｐｒａｇｕｅＤａｗｌｅｙ 雄性大鼠随机分为对照组、抑郁模型组、抑郁模型加电针组和抑郁模型加阿米替林组,每组６ 只。用高效液相电化学法测定大鼠脑内单胺类神经递质及其代谢产物的含量,比较含量的比值。结果　抑郁模型组大鼠脑皮层５羟色胺（５ＨＴ）／５羟吲哚乙酸（５ＨＩＡＡ） 、纹状体多巴胺（ＤＡ）／３,４二羟基苯乙酸（ＤＯＰＡＣ） 分别为０－５０ ±０－１７,１０－３７ ±１－４０,低于对照组（ 分别为０－８８±０－２５ ,１２－３６ ±１－５０）,Ｐ＜ ０－０５ ;皮层去甲肾上腺素（ＮＥ）／５ＨＴ（２－８８ ±１－００） 高于对照组（１－７３±０－４０） ,Ｐ＜ ０－０５。电针刺激百会、印堂穴可使模型大鼠脑皮层５ＨＴ／５ＨＩＡＡ 与ＮＥ／５ＨＴ恢复正常（Ｐ＜０－０５） ,对纹状体ＤＡ／ＤＯＰＡＣ 的降低无影响（ Ｐ＞ ０－０５）。结论　提示电针刺激百会、印堂穴通过降低皮层５ＨＴ的代谢,提高５ＨＴ能神经的活性,并协调ＮＥ 与５ＨＴ之间的平衡来发挥抗抑郁作用。     

ω-3多不饱和脂肪酸对慢性轻度应激鼠海马基因表达的影响

目的 采用基因芯片技术筛选ω-3多不饱和脂肪酸(omega-3 polyunsaturated fatty acids,ω-3PUFAs)对慢性轻度应激(chronic mild stress,CMS)抑郁大鼠海马作用的相关基因.方法 将大鼠根据随机数字表分为3组(6只/组)给予相应处理8周:研究组(ω-3PUFAs 3.1 ml·kg-1·d-1+CMS),模型对照组(生理盐水+CMS)和正常对照组.每周进行行为学指标(体重和糖水摄入量)的测定.采用大鼠10,891条全基因组cDNA芯片,检测研究组(随机取3只大鼠)和模型对照组(全部大鼠)海马的差异表达基因,评价ω-3PUFAs对基因表达的影响.结果 整个试验过程,ω-3PUFAs对体重没有显著影响(P>0.05),试验第7、8周,研究组糖水摄入量高于模型对照组(P<0.01),且与正常对照组无差异(P>0.05).与模型对照组比较.研究组共35条基因有差异表达,其中12条基因上调表达,23条基因下调表达.其中主要包括:转运蛋白基因(Slc 17a9、Rtp4、Slc15a4、Kpnb1、Abcb7),信号转导通路基因(Jun、Strada),电压依赖性离子通道基因(Vdac2).免疫功能蛋白基因(IgE受体β亚单位、IgG2a重链)等.结论 ω-3PUFAs具有抗抑郁作用,其作用机制可能与对转运蛋白、信号转导通路、离子通道、免疫功能蛋白等多类基凶的表达调节有关.     

产后抑郁症与孤啡肽及单胺类递质的相关性研究

目的　探讨孤啡肽 (OFQ)及单胺类递质与产后抑郁症的关系。方法　采用放射免疫法测定 2 5名健康产妇 (对照组 )及 17例产后抑郁症妇女 (抑郁组 )静脉血中孤啡肽及单胺类递质含量。结果　①抑郁组及对照组血孤啡肽含量分别为 (2 7 39± 6 0 4 )ng/L及 (10 37± 3 6 5 )ng/L ,与对照组相比 ,抑郁组孤啡肽含量显著升高 (P <0 0 1) ;抑郁组及对照组血 5 羟色胺 (5 HT)含量分别为 (0 93± 0 2 1) μmol/L及 (1 4 3± 0 36 ) μmol/L ,二者间有显著差异 (P <0 0 5 ) ;抑郁组血多巴胺 (DA)含量为 (2 15± 0 4 1) μmol/L ,显著低于对照组 (P <0 0 5 )。②抑郁组孤啡肽与5 HT及DA含量呈显著负相关 (r为 0 6 0 1及 0 5 93,P <0 0 5 )。③抑郁组爱丁保产后抑郁量表总分 (EPDS)与OFQ含量呈显著正相关 (r为 0 5 12 ,P <0 0 5 ) ,与 5 HT、DA含量呈显著负相关 (r分别为 - 0 5 71及 - 0 5 2 6 ,P <0 0 5 )。结论　孤啡肽与产后抑郁症的发生发展密切相关。     

抑郁症患者脑脊液生长抑素及单胺代谢产物浓度与临床症状的关系

目的 探讨抑郁症患者脑脊液生长抑素（ＳＳ）和单胺代谢产物浓度与临床症状的关系,以及神经递质之间的相互作用。方法 应用放射免疫测定方法和高效液相色谱法,测定２３例抑郁症患者脑脊液ＳＳ和５－羟色胺（５－ＨＴ）代谢产物５－羟吲哚之酸（５－ＨＩＡＡ）、去甲肾上腺素（ＮＥ）代谢产物３－甲基－４－羟－苯乙二醇（ＮＨＰＧ）及多巴胺（ＤＡ）代谢产物高香草酸（ＨＶＡ）的浓度。临床症状评估采用汉密尔顿抑郁量表（ＨＡＭ     

对立违抗性障碍儿童的临床特征及血清单胺类神经递质水平的研究

目的探讨对立违抗性障碍（ODD）患儿的临床特征及血清单胺类神经递质水平的变化。方法对31例ODD儿童（研究组）和36名正常儿童（对照组）测评Piers—Harris儿童自我意识量表（PHCSS）、儿童焦虑性情绪障碍筛查表（SCRED）、儿童抑郁障碍自评量表（DSRSC）及儿童冲动量表（BIS），测量其血清5-羟色胺（5-HT）、多巴胺（DA）等生物胺神经递质的含量。结果（1）研究组PHCSS中的合群性分[（7．36±1．81）分]、幸福与满足感分[（5．45±1．69）分]低于对照组[（8．56±2．50）分和（6．31±1．72）分；P=0．030，P=0．045]。（2）两组SCRED和DSRSC评分的差异无统计学意义（P〉0．05）。研究组BIS的冲动总分[（51．81±9．97）分]、运动分[（8．77±4．11）分]高于对照组[（48．30±11．57）分和（5．19±2．46）分；P=0．020，P：0．000]。（3）研究组血清高香草酸水平[中位数（M）=59nmol／L]、5-HT水平（M=20nmoI／L）低于对照组（M：130nmol／L和168nmoI／L；P=0．024，P=0．033）。（4）血清5-HT水平与冲动总分（r=-0．650）、注意凶子分呈负相关（r=-0．688）；血清DA水平与广泛焦虑冈子呈正相关（r=0．591）；血清5-羟吲哚乙酸水平与分离焦虑因子、社交恐怖因子均呈负相关（r=-0．593，r=-0．535）；血清高香草酸水平与抑郁（r=-0．694）、冲动吲子呈负相关（r=-0．608），均P〈0、05和P〈0．01。结论ODD儿童不合群，缺乏愉快感，冲动性高；其血清5-HT水平降低，而血清儿茶酚歧水平变化不明显。     

慢性应激对大鼠认知及脑脊液单胺类神经递质的影响

目的探讨慢性应激对大鼠脑单胺类神经递质以及认知功能影响的研究。方法75只SD大鼠随机分为对照组(25只)和慢性应激组(50只),后者以束缚浸水应激方式连续应激21天,每日记录大鼠体重及进食量并进行两组比较,三周后行水迷宫实验、大鼠脑单胺类神经递质测定。结果(1)应激组大鼠体重的增加、进食量较对照组明显减少(P<0.05);(2)水迷宫实验:应激组大鼠的游出时间较对照组明显增加(P<0.05),但错误次数无明显差异(P>0.05)。(3)大鼠脑脊液单胺类神经递质含量(ug/L):5-HT、5-HIAA及MHPG的含量应激组明显低于对照组(P<0.05),NA、DA及HVA在应激组均为升高,但无显著差异(P>0.05)。结论慢性束缚浸水应激三周使大鼠脑脊液中5-HT、5-HIAA及MHPG的含量降低,但对认知功能无明显影响。     

香兰素吸嗅对大鼠抑郁样行为及脑单胺类神经递质的影响

目的研究香兰素吸嗅对大鼠抑郁样行为改善及其机制。方法慢性不可预见性中等强度应激(CUMS)+孤养的方法建立大鼠抑郁症模型。为验证香兰素作用途径,另设立大鼠嗅球毁损(OBX)模型。于造模前、后及干预后4 w测试大鼠糖水消耗量和强迫游泳不动时间,干预结束后超高压液相色谱检测大鼠脑内5-HT、DA、NE的量。结果与造模后相比,CUMS+香兰素吸嗅组大鼠神经行为学指标显著好转(P<0.05);其脑匀浆液5-HT、DA的量显著高于空白对照组(P<0.05)。与造模后相比OBX+香兰素吸嗅组大鼠神经行为学指标未见好转(P>0.05);其脑匀浆液5-HT、DA、NE均显著低于假手术组(P<0.05)。结论香兰素可经嗅觉通路改善大鼠抑郁样行为,其机制可能通过提升脑内5-HT、DA实现的。     

不同强度脑电场刺激对抑郁大鼠额叶单胺类递质含量的影响

目的:探讨不同强度脑电场刺激对抑郁大鼠额叶单胺类递质含量的影响。方法:建立Wistar大鼠抑郁症模型;分别在模型大鼠双侧颅骨大脑额叶区放置刺激电极(国家发明专利号ZL01103273.1)并固定,应用脑电场刺激仪给予不同强度脑电场刺激,刺激频率30Hz,刺激波形为正弦波,刺激持续时间1h。应用荧光分光光度法分别测定大鼠额叶脑组织内5羟色胺(5-HT)、去甲肾上腺素(NE)和多巴胺(DA)含量。结果:与正常对照组比,模型对照组大鼠5-HT及NE明显下降(分别P<0.001),治疗对照组单胺类递质无明显变化(分别P>0.05)。低强度治疗组治疗1h后,DA、5-HT及NE含量均无明显改变(分别P>0.05),中等强度治疗组及高强度模型治疗组大鼠额叶脑组织内5-HT及NE含量出现显著增高(分别P<0.05,P<0.01)。结论:一定强度的脑电场刺激可显著提高额叶内单胺类递质的含量,对抑郁症可能提示具有治疗作用。     

大鼠脑缺血对脑微血管及某些脑区单胺类递质水平的影响

为探讨脑微血管中单胺类递质在脑缺血继发性神经元损伤中的作用，用大鼠四血管阻断的脑缺血模型，同时观察脑微血管、脑区单胺类递质在脑缺血、再灌后的变化。单胺类递质有ＨＰＬＣ－ＥＣ法检测。结果表明：不论脑微血管、脑区、单胺类递质含量在缺血与再灌后有不同的变化，如ＮＥ含量在缺血后均为减少，再灌后，脑微血管中继续减少，脑区有不同程度的恢复。提示脑微血管接受单胺能神经支配，单胺能神经参与脑缺血这一病理生理过程。     

大剂量舒肝解郁胶囊对中度抑郁症的疗效及对血清单胺类神经递质和免疫功能的影响

目的观察大剂量舒肝解郁胶囊对中度抑郁症的疗效。方法将160例中度抑郁症患者随机分为对照组和观察组,每组80例;对照组给予常规剂量舒肝解郁胶囊治疗,观察组给予大剂量舒肝解郁胶囊治疗,比较两组治疗效果。结果治疗8周后,观察组较对照组汉密尔顿17项抑郁量表(HAMD-17)评分、汉密尔顿焦虑量表(HAMA)评分明显降低(P<0.05),住院精神病人社会功能评定量表(SSFPI)评分明显升高(P<0.05);治疗8周后,观察组较对照组外周血CD3+、CD4+、CD4+/CD8+及血清多巴胺(DA)、去甲肾上腺素(NE)、5-羟色胺(5-HT)水平明显升高,差异均有统计学意义(P<0.05)。两组不良反应发生率比较(18.75%vs13.75%)无显著差异(χ2=0.735,P<0.05)。结论大剂量舒肝解郁胶囊明显缓解中度抑郁症患者的抑郁症状,改善社会功能,安全性尚可;还可以调节血清单胺类神经递质水平及免疫功能。     

ω-3多不饱和脂肪酸对老年痴呆大鼠学习记忆和海马MDA、SOD的影响

目的 探讨ω-3多不饱和脂肪酸治疗老年痴呆的可能机制.方法 将15月龄健康雌性Wistar大鼠随机分为对照组、痴呆模型组和ω-3多不饱和脂肪酸治疗组[按体质量2.5 g/(kg·d)给予二十碳五烯酸灌胃,共6周],观察大鼠跳台潜伏时间及错误次数,同时测定大鼠海马组织总SOD活力和MDA含量.结果 与痴呆模型组比较,ω-3多不饱和脂肪酸治疗组大鼠的跳台潜伏时间明显延长[分别为(230.88±29.35)s 与 (189.26±31.42)s](P<0.01),触电错误次数减少[分别为(7.3±2.2)次与(9.6±2.2)次](P<0.05),同时其大鼠海马组织总SOD活力增加[分别为(70.19±12.85) U/mg prot与(50.47±14.99) U/mg prot]和MDA含量减少[分别为(7.77±1.57)nmol/mg prot与(9.39±1.44) nmol/mg prot](P<0.05).结论 ω-3多不饱和脂肪酸可改善大鼠学习记忆能力,保护脑组织免遭自由基攻击,在一定程度上为临床治疗老年痴呆提供了实验基础.     

miR-370-3 p对抑郁症大鼠抑郁样行为和神经元损伤的影响

目的 探究miR-370-3p对抑郁症大鼠的抑郁样行为和神经元损伤的影响.方法 采用在线预测软件TargetScan3.1分析miR-370-3p和RUNX1的靶向关系,并通过双荧光素酶报告实验验证其靶向关系,构建过表达miR-370-3p、RUNX1的293T细胞株,采用qPCR和Western blotting分别...     

舒郁胶囊联合尼麦角林对血管性抑郁大鼠的作用及脑单胺类递质受体和载脂蛋白E_4表达的影响

目的探讨舒郁胶囊联合尼麦角林对血管性抑郁(VD)大鼠的作用及脑单胺类递质受体和载脂蛋白E4(ApoE4)表达的影响。方法 48只大鼠随机分为模型组、氟西汀组、舒郁胶囊组、尼麦角林组、舒郁胶囊+尼麦角林组及正常对照组。采用高脂饲养及慢性轻度不可预见性应激制作VD大鼠模型。各组大鼠给予相应的药物或蒸馏水灌胃21 d。各组大鼠于治疗前、后进行敞箱试验、糖水偏嗜试验。大鼠海马5-羟色胺1A受体(5-HT1AR)、多巴胺D2受体(D2DR)、肾上腺素α2A受体(α2AAR)用免疫组化法检测,ApoE4的表达水平用ELISA法检测。结果与正常对照组比较,其他各组VD大鼠治疗前敞箱试验的得分、糖水偏嗜度显著减低(均P0.01);而治疗后各治疗组的上述指标均显著高于模型组(P0.05~0.01),且各治疗组之间的差异无统计学意义。模型组大鼠海马5-HT1AR、D2DR、α2AAR、ApoE4的表达水平明显高于正常对照组,各治疗组大鼠这些指标的表达水平明显低于模型组(均P0.01),且各治疗组之间的差异无统计学意义。结论舒郁胶囊联合尼麦角林对VD大鼠有治疗作用,并使大鼠脑5-HT1AR、D2DR、α2AAR和ApoE4的表达降低。     

基于知信行模式的3H护理对慢性阻塞性肺疾病合并抑郁症患者负性情绪及生活质量的影响

目的探究基于知信行模式的3H护理对慢性阻塞性肺疾病(COPD)合并抑郁症患者负性情绪及生活质量的影响。方法选取2014年2月～2016年9月我院收治的COPD合并抑郁症患者95例,随机分为观察组与对照组,对照组患者采用常规护理,观察组患者采用基于知信行模式的3H护理,对比两组患者负性情绪与生活质量。结果两组患者护理前汉密尔顿抑郁量表(HAMD)评分及焦虑自评量表(SAS)评分相比差异不显著(P0.05),护理后两组患者HAMD评及SAS评分均低于护理前,且观察组患者上述评分均显著低于对照组(P0.05);两组患者护理前临床症状及活动能力评分比较差异无统计学意义(P0.05),护理后两组临床症状及活动能力评分均较护理前有所较低,且观察组明显低于对照组(P0.05)。结论基于知信行模式的3H护理可改善COPD合并抑郁症患者心理状态,提高生活质量。     

脑缺血时半乳糖凝集素-3对大鼠脑皮质中bcl-2、BAX及caspase-3表达的影响

目的通过脑缺血/再灌注损伤模型,测定脑缺血时半乳糖凝集素-3(Gal-3)对B淋巴细胞瘤-2(bcl-2)、Bcl-2相关X蛋白(BAX)及含半胱氨酸的天冬氨酸蛋白水解酶-3(caspase-3)表达的影响,从而为脑缺血的发病机制提供一定的实验依据。方法雄性SD大鼠18只,建立大鼠大脑中动脉阻塞(MCAO)模型,缺血1.5 h,再灌注至24 h。采用随机分组法分为假手术组(sham)、缺血/再灌注组(I/R)和Gal-3 RNA干扰组(siRNA)。采用real-time PCR及western blot检测大鼠脑皮质中Gal-3、bcl-2、BAX及caspase-3 mRNA及蛋白表达变化。结果大鼠脑缺血/再灌注损伤后,脑皮质中Gal-3及bcl-2 mRNA及蛋白表达明显下调,分别为0.38、0.47和1.310、1.299;BAX及caspase-3 mRNA及蛋白表达明显上调,分别为1.41、1.55及1.076、1.155。而Gal-3 RNA干扰后,Gal-3及bcl-2 mRNA及蛋白表达明显下调,分别为0.24、0.14及1.014、1.058;BAX及caspase-3 mRNA及蛋白表达明显上调,分别为1.76、1.88及1.480、1.515。结论 Gal-3可能通过上调bcl-2、下调caspase-3及BAX mRNA及蛋白的表达,参与脑缺血/再灌注损伤的病理过程。     

西酞普兰对慢性应激大鼠海马CA1和CA3区神经细胞B细胞淋巴瘤/白血病-2及Bcl相关蛋白表达与凋亡的影响

Objective To explore effects of citalopram on preventing neuron apoptosis in CA1 and CA3 regions of hippocampus in chronic stress rats.Methods Forty male Sprague Dawley rats were randomly divided into five groups with eight each group.Stressed rat models were made by forced swimming daily for 4 weeks,and the stressed group wag treated with intragagtric administration of 0.9% sodium chloride,and three experimental groups with different dosage of citalopram.The fifth group was given no treatment as control.The proteins of bcl-2 and bax were detected with immunohistochemistry.Apoptosis cell number and integral optical density in CA1 and CA3 regions were tested and analyzed with terminal deoxynucleotidyl transferage biotin-dUTP nick end labeling(TUNEL)method and Nikon imaging software-BR(NIS-BR).Results The stationary time Wag longer in the stress group[(279±53)s]than the control group[(182 ±35)s],and the three citalopram treatment group[(200±71)s,(159±59)s,(165±54)s].The number of struggling[(20 ±3)times]was less than control group[(24 ±3)times]and the treatment groups[(37 ±16),(32 ±10),(24 ±4)times],and exhaustive time[(38.3 ±5.1)min]longer than control group[(22.9±1.8)min],shorter than treatment groups[(54.4 ±2.9)min,(69.3±17.6)min,(46.4±4.0)min].AlJ tIle differences were statistically significant(P＜0.05 or 0.01).Rats in the stress group showed more apoptotic cells,reduced expression of bcl-2 and increased bax protein expression in CA1 and CA3 regions(P＜0.05 or 0.01)in comparison with control group.Compared to the stressed group,rats in treatment groups showed Iess apoptotic cells,reduced expression of bax and increased bcl-2 protein expression in CA1 and CA3 regions(P＜0.05).Conclusion Long-term stress might cause neuron apoptosis and expression of bcl-2 and bax in CA1 and CA3 region of hippocampus,and citalopram might have prophylactic effects on this process.     

西酞普兰对慢性应激大鼠海马CA1和CA3区神经细胞B细胞淋巴瘤/白血病-2及Bcl相关蛋白表达与凋亡的影响

Objective To explore effects of citalopram on preventing neuron apoptosis in CA1 and CA3 regions of hippocampus in chronic stress rats.Methods Forty male Sprague Dawley rats were randomly divided into five groups with eight each group.Stressed rat models were made by forced swimming daily for 4 weeks,and the stressed group wag treated with intragagtric administration of 0.9% sodium chloride,and three experimental groups with different dosage of citalopram.The fifth group was given no treatment as control.The proteins of bcl-2 and bax were detected with immunohistochemistry.Apoptosis cell number and integral optical density in CA1 and CA3 regions were tested and analyzed with terminal deoxynucleotidyl transferage biotin-dUTP nick end labeling(TUNEL)method and Nikon imaging software-BR(NIS-BR).Results The stationary time Wag longer in the stress group[(279±53)s]than the control group[(182 ±35)s],and the three citalopram treatment group[(200±71)s,(159±59)s,(165±54)s].The number of struggling[(20 ±3)times]was less than control group[(24 ±3)times]and the treatment groups[(37 ±16),(32 ±10),(24 ±4)times],and exhaustive time[(38.3 ±5.1)min]longer than control group[(22.9±1.8)min],shorter than treatment groups[(54.4 ±2.9)min,(69.3±17.6)min,(46.4±4.0)min].AlJ tIle differences were statistically significant(P＜0.05 or 0.01).Rats in the stress group showed more apoptotic cells,reduced expression of bcl-2 and increased bax protein expression in CA1 and CA3 regions(P＜0.05 or 0.01)in comparison with control group.Compared to the stressed group,rats in treatment groups showed Iess apoptotic cells,reduced expression of bax and increased bcl-2 protein expression in CA1 and CA3 regions(P＜0.05).Conclusion Long-term stress might cause neuron apoptosis and expression of bcl-2 and bax in CA1 and CA3 region of hippocampus,and citalopram might have prophylactic effects on this process.     

西酞普兰对慢性应激大鼠海马CA1和CA3区神经细胞B细胞淋巴瘤/白血病-2及Bcl相关蛋白表达与凋亡的影响

Objective To explore effects of citalopram on preventing neuron apoptosis in CA1 and CA3 regions of hippocampus in chronic stress rats.Methods Forty male Sprague Dawley rats were randomly divided into five groups with eight each group.Stressed rat models were made by forced swimming daily for 4 weeks,and the stressed group wag treated with intragagtric administration of 0.9% sodium chloride,and three experimental groups with different dosage of citalopram.The fifth group was given no treatment as control.The proteins of bcl-2 and bax were detected with immunohistochemistry.Apoptosis cell number and integral optical density in CA1 and CA3 regions were tested and analyzed with terminal deoxynucleotidyl transferage biotin-dUTP nick end labeling(TUNEL)method and Nikon imaging software-BR(NIS-BR).Results The stationary time Wag longer in the stress group[(279±53)s]than the control group[(182 ±35)s],and the three citalopram treatment group[(200±71)s,(159±59)s,(165±54)s].The number of struggling[(20 ±3)times]was less than control group[(24 ±3)times]and the treatment groups[(37 ±16),(32 ±10),(24 ±4)times],and exhaustive time[(38.3 ±5.1)min]longer than control group[(22.9±1.8)min],shorter than treatment groups[(54.4 ±2.9)min,(69.3±17.6)min,(46.4±4.0)min].AlJ tIle differences were statistically significant(P＜0.05 or 0.01).Rats in the stress group showed more apoptotic cells,reduced expression of bcl-2 and increased bax protein expression in CA1 and CA3 regions(P＜0.05 or 0.01)in comparison with control group.Compared to the stressed group,rats in treatment groups showed Iess apoptotic cells,reduced expression of bax and increased bcl-2 protein expression in CA1 and CA3 regions(P＜0.05).Conclusion Long-term stress might cause neuron apoptosis and expression of bcl-2 and bax in CA1 and CA3 region of hippocampus,and citalopram might have prophylactic effects on this process.     

西酞普兰对慢性应激大鼠海马CA1和CA3区神经细胞B细胞淋巴瘤/白血病-2及Bcl相关蛋白表达与凋亡的影响

Objective To explore effects of citalopram on preventing neuron apoptosis in CA1 and CA3 regions of hippocampus in chronic stress rats.Methods Forty male Sprague Dawley rats were randomly divided into five groups with eight each group.Stressed rat models were made by forced swimming daily for 4 weeks,and the stressed group wag treated with intragagtric administration of 0.9% sodium chloride,and three experimental groups with different dosage of citalopram.The fifth group was given no treatment as control.The proteins of bcl-2 and bax were detected with immunohistochemistry.Apoptosis cell number and integral optical density in CA1 and CA3 regions were tested and analyzed with terminal deoxynucleotidyl transferage biotin-dUTP nick end labeling(TUNEL)method and Nikon imaging software-BR(NIS-BR).Results The stationary time Wag longer in the stress group[(279±53)s]than the control group[(182 ±35)s],and the three citalopram treatment group[(200±71)s,(159±59)s,(165±54)s].The number of struggling[(20 ±3)times]was less than control group[(24 ±3)times]and the treatment groups[(37 ±16),(32 ±10),(24 ±4)times],and exhaustive time[(38.3 ±5.1)min]longer than control group[(22.9±1.8)min],shorter than treatment groups[(54.4 ±2.9)min,(69.3±17.6)min,(46.4±4.0)min].AlJ tIle differences were statistically significant(P＜0.05 or 0.01).Rats in the stress group showed more apoptotic cells,reduced expression of bcl-2 and increased bax protein expression in CA1 and CA3 regions(P＜0.05 or 0.01)in comparison with control group.Compared to the stressed group,rats in treatment groups showed Iess apoptotic cells,reduced expression of bax and increased bcl-2 protein expression in CA1 and CA3 regions(P＜0.05).Conclusion Long-term stress might cause neuron apoptosis and expression of bcl-2 and bax in CA1 and CA3 region of hippocampus,and citalopram might have prophylactic effects on this process.