首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到19条相似文献,搜索用时 156 毫秒
1.
目的 探讨电针对失眠大鼠下丘脑食欲素A(orexinA)的影响及不同强度电针对orexinA的效应差异。方法将SD大鼠随机分为正常对照组(normalcontrol,NC)、失眠模型组(insomniamodel,IM)、强刺激电针组(strongstimulativeeleetroacupuncture,SSEA)、弱刺激电针组(weakstimulativeelectroacupuncture,WSEA)。除正常对照组外,其余各组大鼠均用对氯苯丙氨酸(PCPA)建立大鼠失眠模型,选穴“百会”、“足三里”、“三阴交”,并用不同强度电针治疗。5d后,用逆转录一聚合酶链反应(RT-PCR)检测下丘脑orexinAmRNA表达,采用免疫组织化学技术观察下丘脑orexinA阳性神经元表达。结果与正常对照组比较,失眠模型组大鼠下丘脑orexinAmRNA表达显著升高(P〈0.01),orexinA阳性神经元染色较深,且表达量较多;与失眠模型组相比,两电针组大鼠下丘脑orexinAmRNA表达明显下降(P〈0.01),orexi—nA阳性神经元染色较浅,表达量较少,强刺激电针组作用更为明显。结论电针可以改善失眠大鼠下丘脑异常增多的orexinA,调节睡眠-觉醒周期,且强刺激电针组效果较好。  相似文献   

2.
本实验旨在研究生地黄水提物对大鼠睡眠的影响,并探讨其可能的作用机制。参照《保健食品功能检验与评价方法》(2022版)中有助于改善睡眠的检验方法初步评价生地黄水提物的效果。进一步建立失眠大鼠模型,检测各给药组大鼠下丘脑中枢神经递质及相应受体的mRNA表达水平,并检测大鼠血清中炎症因子含量。结果显示生地黄水提物能改善大鼠睡眠且安全性良好,并且能显著增加失眠大鼠下丘脑中γ-氨基丁酸(gamma-aminobutyric acid, GABA)和5-羟色胺(5-hydroxytryptamine, 5-HT)含量,显著降低谷氨酸(glutamic acid, Glu)和多巴胺(dopamine, DA)含量,相应神经递质的受体mRNA表达量也发生同样的变化趋势,此外给药组大鼠血清中细胞炎症因子TNF-α、IL-1β含量显著下降,IL-10的含量显著增加。说明生地黄水提物可通过调节神经递质和细胞炎症因子改善大鼠睡眠。  相似文献   

3.
不同强度电针对肥胖大鼠脂肪组织炎症相关因子的影响   总被引:1,自引:0,他引:1  
探讨不同强度电针对肥胖大鼠脂肪组织核因子-κBp65(NF-κBp65)、单核细胞趋化蛋白-1(MCP-1)和肿瘤坏死因子-α(TNF-α)的作用差异.将SD大鼠随机分为普通饮食组、高脂饮食组、5 V电针组、2.5 V电针组,除普通饮食组外其余各组大鼠均饲以高脂饲料.取"足三里"、"三阴交"穴,不同强度电针治疗14 d后,用蛋白质印迹技术(Western blot)检测肥胖大鼠附睾脂肪组织NF-κBp65的表达,酶联免疫吸附法(ELISA)检测肥胖大鼠附睾脂肪组织MCP-1、TNF-α的含量.研究发现两电针组肥胖大鼠体重、Lee’s指数、脂肪组织中NF-κBp65表达、MCP-1和TNF-α含量较高脂饮食组显著降低(P<0.01),5 V电针组较2.5 V电针组下降效果更为明显(P<0.01,P<0.05).结果表明电针可改善肥胖脂肪组织炎症反应状态,减轻肥胖大鼠体重,且5 V电针组效果优于2.5 V电针组.  相似文献   

4.
采用逆转录-聚合酶链式反应检测了慢性足底电击结合噪声应激致高血压大鼠下丘脑、延髓、中脑、垂体和肾上腺等组织中编码肾上腺髓质素的肾上腺髓质素前肽原(preproadrenomedullin,ppADM)基因以及ADM的特异性受体组件降钙素受体样受体(calcitonin-receptor-like receptor,CRLR)和受体活性调节蛋白2和3(receptor-activty-modifying proteins,RAMP2和RAMP3)表达的变化.我们观察到:与对照组相比,以3-磷酸甘油醛脱氢酶作为内参照,15 d足底电击结合噪声应激引起下丘脑、垂体和肾上腺中ppADM mRNA表达上调,而在延髓和中脑表达明显下调(P<0.01或P<0.05);CRLR基因表达量正常时在下丘脑相对较高,应激15 d后CRLR表达在延髓、中脑和下丘脑下调(P<0.01或P<0.05),而在垂体和肾上腺的表达无明显变化;应激后RAMP2基因在延髓和下丘脑表达上调,而在肾上腺表达显著下调(P<0.01),其他部位无明显变化;RAMP3基因在对照组大鼠的中脑和下丘脑表达较高,在应激性高血压大鼠的下丘脑和垂体表达上调(P<0.01或P<0.05),而在中脑和肾上腺表达下调(P<0.05),在延髓中的表达变化无统计学差异.上述结果提示:慢性足底电击结合噪声应激引起明显的中枢和下丘脑-垂体-肾上腺轴ADM及其受体组件CRLR/RAMP2或CRLR/RAMP3基因的表达变化.但慢性应激后中枢源性ADM及其受体的表达变化对应激和血压的调节以及在应激致高血压中的确切作用及机制尚待进一步研究.  相似文献   

5.
目的探讨褪黑素(melatonin,MT)对谷氨酸(glutamate,Glu)致痫大鼠海马内Glu及GluR2、γ-氨基丁酸(γ-aminobutyric-acid,GABA)及其受体GABRA1水平的影响,进而研究褪黑素的抑痫作用机制。方法随机将健康SD雄性大鼠40只分为A、B、C、D组,每组10只。A组:生理盐水组;B组:MT Glu组;C组:Glu致痫组;D组:Luzidole MT Glu组。观察并记录行为学变化,采用免疫组化法进行Glu、GluR2、GABA和GABRA1免疫组化染色和图像分析。结果行为学观察结果显示,C组和D组大鼠均有不同程度的癫痫发作,B组大鼠癫痫发作不明显,A组无发作;免疫组化结果显示,C组和D组海马内CA1-CA3区和齿状回Glu阳性反应较A组增强(P<0.05),GluR2、GABA和GABRA1均较A组减弱(P<0.05),B组Glu较C组和D组阳性反应有显著性减弱(P<0.05),GluR2、GABA和GABRA1阳性反应均较C组和D组有显著性增强(P<0.05),而B组与A组无明显差异性。结论MT通过增加GABA及其受体GABRA1和GluR2的作用和抑制Glu作用对Glu致痫大鼠癫痫发作发挥抑制作用。  相似文献   

6.
针刺穴位对脑缺血再灌注大鼠脑内NMDA R1 mRNA的影响   总被引:9,自引:0,他引:9  
采用大鼠大脑中动脉栓塞为局灶性脑缺血模型,以针刺穴位为治疗手段,用原位杂交技术显示NMDAR1 mRNA,探讨单纯缺血,缺血加电针治疗后脑内NMDAR1mRNA的变化,并用谷氨酸或MK-801兴奋或桔抗NMDA受体。观察对便塞灶的影响。探讨NMDA受体在脑缺血脑损伤中的作用。结果显示:(1)谷氨酸能显著增大脑梗塞面积,电针能明显缩小梗塞面积,MK-801与电针作用相似,也能缩小梗塞面积,与对照组相比,谷氨酸组,电针组和MK-801组均有显著性差异;(2)缺血侧海马及大脑皮层NMDAR1 mRNA阳性细胞明显高于对照侧,两者间有显著性差异(P<0.01);经电针治疗后,NMDAR1 mRNA无过表达现象,海马及大脑皮层缺血侧NMDAR1 mRNA阳性细胞数与对照侧相比无显著性差异,但明显低于单纯缺血组(P<0.01)。以以结果表明,谷氨酸介导的缺血性脑损伤的机制之一是通过NMDAR1 mRNA的过表达而实现的,电针对脑缺血性神经元损伤的保护作用可通过抑制NMDAR1 mRNA的过表达而实现。  相似文献   

7.
目的 探讨胰岛素对急性肺损伤(ALI)大鼠肺血管内皮细胞核因子-kB(NF-kB)和细胞问粘附分子-1(ICAM-1)表达的影响.方法 24只健康雄性SD大鼠(190-210g),随机分为正常对照组、All模型组、胰岛素干预组.观察肺组织病理形态,采用原位杂交技术半定最法和免疫组织化学染色检测肺血管内皮细胞的细胞间粘附分子-1(ICAM-1)mRNA和核因子-kB(NF-kB)蛋白的表达.结果 (1)肺病理组织学结果显示胰岛素干预组肺病变局限且程度减轻;(2)ALI模型组肺血管内皮细胞ICAM-1mRNA表达(0.456±0.018)和NF-kB核染色阳性细胞百分比(0.542±0.009)与正常对照组(0.274±0.014,0.308±0.017)比较显著升高(均P<0.05);(3)胰岛素干预组ICAM-1mRNA表达(0.357±0.024)和NF-KB核染色阳性细胞了百分比(0.427±0.018)比模型组明显减低(均P<0.05),但与正常对照组比较仍较高(均P<0.05).结论 ICAM-1和NF-kB在ALI显著增加,胰岛素可以抑制NF-kB和ICAM-ImRNA的表达,可能足其对抗ALI的作用机制之一.  相似文献   

8.
目的通过建立MSG-肝再生-大鼠模型,检测MSG-肝再生-大鼠下丘脑弓状核(ARN)TGF-β1 mRNA的表达与神经内分泌免疫网络的关系.方法用肝大部分切除MSG-大鼠的方法建立MSG-肝再生-大鼠模型,原位杂交技术检测MSG-肝再生-大鼠下丘脑弓状核(ARN)TGF-β1 mRNA的表达.结果发现MSG-肝再生-大鼠ARN TGF-β1mRNA的表达显著上调,切除11天达20.9±1.6,与生理盐水组(11.1±1.2)和MSG-大鼠假手术组(15.2±1.1)比较,差异显著(P<0.01).结论 MSG-肝再生-大鼠神经-内分泌-免疫网络功能紊乱与其ARN TGF-β1 mRNA表达失调密切相关.  相似文献   

9.
目的检测γ-氨基丁酸(gamma-aminobutyric acid,GABA)和谷氨酸脱羧酶(glutamic acid decarboxylase,GAD)在大鼠降结肠上皮的表达及分布特征,并探讨GABA与上皮细胞分化增殖的关系。方法用免疫荧光及激光共聚焦显微扫描技术,检测GABA、GAD65及GAD67在大鼠降结肠上皮中的表达,并以麦芽凝聚素组织化学染色与免疫荧光结合的双重染色显示GABA和GAD65表达细胞的分布特征。同时,用RT-PCR方法检测GAD mRNA的表达。此外,用3H-胸腺嘧啶放射自显影及增殖细胞核抗原(PCNA)免疫组化方法显示降结肠上皮的增殖带。结果RT-PCR显示降结肠粘膜中GAD65及GAD67mRNA均为阳性。GABA及GAD65免疫反应阳性细胞主要分布在降结肠的腔面和隐窝的上1/3上皮细胞的胞浆,而GAD67阳性细胞仅分布腔面,此外,GABA及GAD65阳性染色也见于黏膜固有层。双重染色显示杯状细胞中GABA及GAD65均为阴性3。H-胸腺嘧啶及PCNA标记阳性细胞主要在隐窝的中下段。结论GABA及GAD65分布在大鼠降结肠上皮的成熟带及功能带,GABA系统可能参与上皮细胞的分化与增殖的调节。  相似文献   

10.
目的: 探讨丁苯酞对慢性睡眠剥夺后大鼠脑部额叶小胶质细胞活化及炎症因子的影响。方法: 本实验共分为4组(n=8):空白对照组、大平台对照组、慢性睡眠剥夺组、丁苯酞干预组。慢性睡眠剥夺组和丁苯酞干预组采用改良多平台睡眠剥夺法建立大鼠慢性睡眠剥夺模型,对大鼠进行每日18 h,连续28 d的睡眠剥夺。在这28 d内,空白对照组大鼠不进行睡眠干预,大平台对照组大鼠放于大平台箱内。丁苯酞干预组在睡眠剥夺28 d结束后按100 mg/kg腹腔注射丁苯酞针剂,每日1次,共14 d,其他组大鼠在这14 d内腹腔注射同样剂量的生理盐水。腹腔注射结束后各组大鼠取脑组织,免疫组化检测额叶皮质离子钙接头分子(Iba-1)阳性细胞并计数,Western blot检测额叶诱导型一氧化氮合成酶(iNOS)、精氨酸酶1(Arg1)表达,实时定量PCR检测额叶白介素-1(IL-1)mRNA、IL-6 mRNA、肿瘤坏死因子-α(TNF-α) mRNA。结果: 与空白对照组、大平台对照组比较,慢性睡眠剥夺组额叶Iba-1阳性细胞体积增大伴细胞突起增多,且细胞数增加(P均<0.05),iNOS和IL-1 mRNA、IL-6 mRNA、TNF-α mRNA表达增加,而Arg1表达减少(P均<0.05);与慢性睡眠剥夺组比较,丁苯酞干预组额叶Iba-1细胞数减少(P< 0.05),iNOS和IL-1 mRNA、IL-6 mRNA、TNF-α mRNA表达减少(P均<0.05)而Arg1表达无明显改变。结论: 丁苯酞可抑制慢性睡眠剥夺导致的大鼠额叶小胶质细胞活化、减少慢性睡眠剥夺后的炎症因子表达。  相似文献   

11.
为探讨朱茯苓治疗失眠的可能作用机制,通过TCMSP、BAT-MAN、TCMID和STITCH数据库以及文献挖掘筛选朱茯苓的活性成分及潜在靶点,利用TTD、OMIM、GeneCards和CTD数据库获取失眠类疾病的相关靶点,采用Cytoscape软件和String数据库构建活性成分-靶点网络和靶点蛋白相互作用网络,通过BioGPS数据库进行靶点的器官定位,基于David数据库进行GO功能和KEGG通路的富集分析,利用Autodock_vina软件进行活性成分和核心靶点的分子对接验证,最后通过免疫印迹法(Western blot)验证朱茯苓对γ-氨基丁酸(GABA)的两种受体蛋白α1亚基基因GABRA1和γ2亚基基因GABRG2的影响。最终筛选得到朱茯苓活性成分33种,潜在靶点267个,与失眠的交集靶点36个,多作用于脑、心脏等器官;分子对接结果显示GABRA1、GABRG2两个靶点能够与活性成分自发结合并借助氢键等分子间作用力形成较为稳定的构象;富集分析共获得189个GO条目和24条KEGG通路,主要涉及GABA信号通路、5-羟色胺(5-HT)信号通路等;Western blot实验证明朱茯苓能够增强小鼠脑内GABRA1和GABRG2蛋白的表达。通过网络药理学、分子对接和Western blot实验验证,发现朱茯苓可能通过多成分、多靶点、多途径的协同作用发挥镇静安神的作用,为深入进行朱茯苓治疗失眠的作用机制研究提供新思路和新方法。  相似文献   

12.
目的研究促甲状腺激素释放激素受体-1(thyrotrophin-releasing hormone receptor type-1, TRH-R1)在大鼠睾丸出生后不同发育阶段的表达,探讨其在生殖发育调节中的作用.方法应用蛋白质免疫印迹杂交技术以及免疫组织化学ABC法检测TRH-R1在8d、15d、20d、35d、60d和90d大鼠睾丸中的表达和定位,并结合图像分析技术对免疫组化结果进行统计学分析观察其在发育过程中的变化.结果免疫印迹杂交发现TRH-R1蛋白表达于15d以后各阶段的大鼠睾丸;而运用免疫组化在第8d即检测到TRH-R1的表达,以后发育过程中的各个阶段均有阳性反应细胞, TRH-R1定位于大鼠睾丸的间质细胞;免疫反应阳性物均位于胞膜和胞质,胞核区为阴性;图像分析结果表明,随着大鼠睾丸的发育,TRH-R1表达量呈增多趋势,且具有统计学差异(P<0.01).结论本实验证明TRH-R1在出生后8d大鼠的睾丸内即有表达,并持续表达于其后各个发育阶段;TRH-R1定位于睾丸的间质细胞,其表达量随着增龄变化呈增多趋势,即同发育过程相关.  相似文献   

13.
Migraine is a debilitating neurovascular disorder, with a substantial genetic component. The exact cause of a migraine attack is unknown; however cortical hyperexcitability is thought to play a role. As Gamma-aminobutyric Acid (GABA) is the major inhibitory neurotransmitter in the brain, malfunctioning of this system may be a cause of the hyperexcitability. To date, there has been limited research examining the gene expression or genetics of GABA receptors in relation to migraine. The aim of our study was to determine if GABA receptors play a role in migraine by investigating their gene expression using profile in migraine affected individuals and non-affected controls by Q-PCR. Gene expression of GABA(A) receptor subunit isoforms (GABRA3, GABRB3, GABRQ) and GABA(B) receptor 2 (GABBR2) was quantified in mRNA obtained from peripheral blood leukocytes from 28 migraine subjects and 22 healthy control subjects. Analysis of results showed that two of the tested genes, GABRA3 and GABBR2, were significantly down regulated in migraineurs (P=0.018; P=0.017), compared to controls. Results from the other tested genes did not show significant gene expression variation. The results indicate that there may be specific GABA receptor gene expression variation in migraine, particularly involving the GABRA3 and GABBR2 genes. This study also identifies GABRA3 and GABBR2 as potential biomarkers to select migraineurs that may be more responsive to GABA agonists with future investigations in this area warranted.  相似文献   

14.
15.
γ-氨基丁酸(gamma-aminobutyric acid,GABA)是哺乳动物中枢神经系统主要的抑制性神经递质,并具有调节血压与心率、调节情绪、抗焦虑、抗抑郁、抗肿瘤、保肝护肾、调节激素分泌等生理功能。目前主要通过厌氧等技术处理植物原料、微生物发酵以及外源添加的方式加工富含GABA的食品,涉及富含GABA的茶叶、粮食、豆类制品、乳制品、糖果、饮料等食品的研究、专利及部分产品,但产品较少,今后需加强产业化。  相似文献   

16.
Gamma-aminobutyric acid (GABA) participates in neuroendocrine regulation. Since steroid hormones have been shown to modulate the GABAergic system, here we evaluated the effect of chronic in vivo estradiol administration on GABA B receptor (GABA(B)R) expression. GABA(B1) and GABA(B2) subunits were analyzed by Western Blot and RT-PCR, in hypothalami and anterior pituitaries of adult female rats: a) treated for 1 week with estradiol-valerate (a single dose of 100 mug /kg: E1), b) implanted with a 10 mg pellet of estradiol-benzoate for 5 weeks (E5) or c) on proestrous (P), d) ovariectomized (OVX). Pituitary GABA(B)R levels were correlated to a biological effect: baclofen, a GABA(B)R agonist, action on intracellular calcium titers ([Ca(2+)](i)) in pituitary cells. E5 pituitaries showed a significant decrease in the expression of GABA(B1) and GABA(B2) mRNAs compared to P. The GABA(B1a) splice variant of GABA(B1) was always more abundant than GABA(B1b) in this tissue. Similar to the pituitary, hypothalamic GABA(B1) and GABA(B2) mRNAs decreased in E5; this was confirmed at the protein level. In the hypothalamus GABA(B1b) was the main variant expressed in P rats, and was the one significantly sensitive to estradiol-induced decrease, as determined by Western Blots. Castration did not modify GABA(B)R expression with regards to P in either tissue. In P pituitary cells baclofen induced a decrease in [Ca(2+)](i), in contrast this effect was lost in E5 cells. We conclude that chronic estradiol treatment negatively regulates the expression of the GABA(B)R subunits in the pituitary and the hypothalamus. This effect is coupled to a loss of baclofen action on intracellular calcium in pituitary cells.  相似文献   

17.
建立一种快速、准确、可靠的γ 氨基丁酸定量检测方法 ,并观察高原低氧大鼠下丘脑γ 氨基丁酸 (GABA)含量变化。采用 6 30 0黄金系统氨基酸分析仪 ,在锂柱 130min程序生理体液分析方法基础上 ,根据γ 氨基丁酸 (GABA)的特性 ,建立了GABA的快速测定方法 ,并用此方法检测了高原低氧条件下大鼠下丘脑GABA的含量变化。结果高原低氧组大鼠下丘脑GABA的含量明显增多。此方法分析GABA的保留时间为 8.87min ,比原方法缩短了 6 5 .96min ;并且有较好的重现性 (CV :1.39% )、回收率高 (98.81% )。是一种快速、准确、可靠的GABA定量检测方法 ,可用于大批量样品的快速测定  相似文献   

18.
Brain GABA levels rise and plateau following prolonged administration of the irreversible GABA-transaminase inhibitor vigabatrin (γ-vinylGABA). Recently it has been shown that increased GABA levels reduces GAD67 protein, one of two major isoforms of glutamic acid decarboxylase (GAD). The effects of GABA elevation on GABA synthesis were assessed in vivo using1H and13C-edited NMR spectroscopy. Rates of turnover of cortical glutamate and GABA from intravenously administered [1-13C]glucose were measured in α-chloralose anesthetized rats 24 hours after receiving vigabatrin (500 mg/kg, i.p.) and in non-treated controls. GABA concentration was increased 2-fold at 24 hours (from 1.3±0.4 to 2.7±0.9 μmol/g) and GABA-T activity was inhibited by 60%. Tricarboxylic acid cycle flux was not affected by vigabatrin treatment compared to non-treated rats (0.47±0.19 versus 0.52±0.18 μmol/g, respectively). GABA-C2 fractional enrichment (FE) measured in acid extracts rose more slowly in vigabatrin-treated compared to nontreated rats, reaching >90% of the glutamate FE after 3 hours. In contrast, GABA FE≥glutamate FE in non-treated rats. A metabolic model consisting of a single glutamate pool failed to account for the rapid labeling of GABA from glutamate. Metabolic modelling analysis based on two (non-communicating) glutamate pools revealed a ∼70% decrease in the rate of GABA synthesis following vigabatrin-treatment, from 0.14 (non-treated) to 0.04 μmol/g/min (vigabatrin-treated). These findings, in conjunction with the previously reported differential effects of elevated GABA on the GAD isoforms, suggests that GAD67 may account for a major fraction of cortical GABA synthesis in the α-chloralose anesthetized rat brain in vivo. Special issue dedicated to Dr. Herman Bachelard.  相似文献   

19.
We have previously shown that GABA protects pancreatic islet cells against apoptosis and exerts anti-inflammatory effects. Notably, GABA inhibited the activation of NF-κB in both islet cells and lymphocytes. NF-κB activation is detrimental to beta cells by promoting apoptosis. However, the mechanisms by which GABA mediates these effects are unknown. Because the above-mentioned effects mimic the activity of sirtuin 1 (SIRT1) in beta cells, we investigated whether it is involved. SIRT1 is an NAD+-dependent deacetylase that enhances insulin secretion, and counteracts inflammatory signals in beta cells. We found that the incubation of a clonal beta-cell line (rat INS-1) with GABA increased the expression of SIRT1, as did GABA receptor agonists acting on either type A or B receptors. NAD+ (an essential cofactor of SIRT1) was also increased. GABA augmented SIRT1 enzymatic activity, which resulted in deacetylation of the p65 component of NF-κB, and this is known to interfere with the activation this pathway. GABA increased insulin production and reduced drug-induced apoptosis, and these actions were reversed by SIRT1 inhibitors. We examined whether SIRT1 is similarly induced in newly isolated human islet cells. Indeed, GABA increased both NAD+ and SIRT1 (but not sirtuins 2, 3 and 6). It protected human islet cells against spontaneous apoptosis in culture, and this was negated by a SIRT1 inhibitor. Thus, our findings suggest that major beneficial effects of GABA on beta cells are due to increased SIRT1 and NAD+, and point to a new pathway for diabetes therapy.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号