皮层抑制对大鼠丘脑底核自发放电的影响

目的:观察皮层抑制对正常及帕金森病(PD)大鼠丘脑底核(STN)神经元自发放电的影响。方法:采用玻璃微电极细胞外记录法,观察正常和PD大鼠STN神经元的放电活动及脑内微量注射KCl后,两组大鼠STN神经元放电频率的变化。结果:对照组和PD组大鼠STN神经元放电频率分别为(9.78±0.71)Hz和(23.81±1.08)Hz,PD组大鼠放电频率显著高于对照组(P<0.01),且呈爆发式放电的神经元比例明显高于对照组(P<0.05)。皮层注射KCl后,经过较长的潜伏期,两组大鼠STN神经元放电频率均明显降低,后缓慢恢复。结论:PD大鼠STN神经元放电频率增高,爆发式放电增多,而抑制皮层可使这种异常放电得到改善,提示皮层兴奋性的改变可能是PD中STN活动增强的另一个诱因。     

多通道在体记录技术——神经元放电与节律性场电位间的相位分析方法

本文旨在介绍神经元放电序列与节律性场电位间的相位分析方法。多通道在体记录技术能同时记录群体神经元和局部场电位的活动信号。神经元的放电活动一般表征为放电时间序列;而在局部场电位信号中,则包含有不同频率成分的周期性节律振荡。相位分析主要考察神经元放电时刻与周期性节律场电位相位间的相互关系。具体分析时,先运用Hilbert变换计算出某一频段节律场电位信号的瞬时相位值,然后再计算某一神经元放电序列中每个动作电位相对于该节律场电位的放电相位,最后通过考察这些放电相位的分布特性,来判断该神经元与该节律场电位相位间的放电相位关系。如一神经元放电序列对某种节律场电位的相位分布经统计检验不是随机的,则表明该神经元对这种节律场电位有放电锁相关系。Theta相位进动则是一种特殊的神经元放电与周期性节律场电位间的相位关系,也是海马位置细胞放电的基本特性之一。海马位置细胞在位置野内一般呈theta节律簇状放电模式,而相位进动是指每一theta波内放电的theta相位,相对上一theta波会逐渐提前。这一现象可通过对位置细胞放电的theta相位和动物实时位置使用线性模型来描述;并运用圆周线性相关分析法,计算它们之间的相关系数,从而研究位置细胞在位置野中的放电相对于theta相位的进动情况。通过相位分析,可以帮助我们了解神经元放电与节律性场电位信号间的时间信息编码特性。     

青霉素致痫大鼠海马神经元单位放电特征分析

目的:观察青霉素致痫大鼠海马神经元单位放电特征。方法:24只Wistar雄性健康大鼠,随机分为正常对照组、癫痫模型组各12只。癫痫模型组用青霉素钠按6×106U/kg腹腔注射,观察癫痫发作级别,记录海马神经元单位放电。结果:正常对照组大鼠共记录到24个单位海马神经元放电,放电频率以中低频放电为主,放电形式以单个不均匀放电为主;癫痫模型组共记录到78个单位海马神经元放电,放电频率以高频放电为主,放电形式则以混合型放电为主,癫痫发作程度强。癫痫模型组与正常对照组比较,海马神经元单位放电数、放电频率以及放电形式均有显著性差异(P0.01);结论:青霉素诱导的癫痫模型,海马神经元单位放电数明显增多,放电频率高,并以混合型爆发放电为主。     

延髓头端腹外侧区神经元电活动与心血管活动相干性的研究

本文分析了大鼠延头端腹外侧区（ＲＶＬＭ）神经元单位活动与心血管活动的相干性,观察了ＲＶＬＭ区神经元电 对电刺激中脑防御反应区的诱发反应,以及对压力感受性反射的反应,并用ＦＦＴ对ＲＶＬＭ区神经元自发单位放电和血压波进行频域的相干性分析,以判断是具有心节律。还分析了ＲＶＬＭ区单位放电变异性与心率变异性的相干性。结果显示：ＲＶＬＭ区大多数神经元对电刺激中脑防御反应区呈兴奋反应（６７％）,７０％神经元放电     

孕期家装污染对子代大鼠脑组织结构和认知功能的影响

目的:建立孕期家装污染大鼠模型,并探讨其对孕鼠子代神经元形态和神经行为的影响.方法:将22只成年孕鼠随机分为对照组和染毒组,分别在孕早期(D1-D10)给予相应的处理.在生后不同时间观察新生大鼠大脑的发育并检测脑组织重量,同时观察新生大鼠皮层神经元的形态变化并检测学习记忆活动.结果:各组新生大鼠脑组织无畸形,且各组大鼠脑组织重量无显著变化,但与对照组相比染毒组皮层神经元的排列及形态欠规则.出生一月后染毒组皮层神经元突起的数量及长度均少于对照组.行为学检测观察到染毒组大鼠其子代大鼠的学习记忆能力明显低于对照组.结论:家装污染物可导致新生大鼠海马神经元的形态学改变并抑制神经元突起的发育与生长,对大鼠的学习记忆功能有明显的损害作用.     

5,7-双羟色胺侧脑室注射对大鼠内侧前额叶皮层神经元兴奋性的影响

本研究采用在体细胞外记录的方法,探讨了双侧侧脑室注射5,7-双羟色胺(5,7-dihydroxytryptamine,5,7-DHT)损毁大鼠脑内5-羟色胺(5-hydroxytryptamine,5-HT)神经元后,内侧前额叶皮层(medial prefrontal cortex,m PFC)锥体和中间神经元兴奋性的变化。实验结果显示:5,7-DHT注射到双侧侧脑室后第2周,m PFC和中缝背核内的5-HT水平较正常组显著下降。m PFC的锥体神经元的放电频率与正常组相比明显升高,爆发式放电显著增多,而中间神经元的平均放电频率显著降低,放电形式趋向不规则活动。结果提示5-HT能递质系统对m PFC神经元活动具有重要的调节作用。     

氟桂利嗪对青霉素致痫大鼠皮层及海马癫痫样放电的影响

目的:观察氟桂利嗪对青霉素致痫大鼠皮层和海马癫痫样放电的影响.方法:选取Wistar大鼠60只制作青霉素致痫模型,在大鼠海马、颞叶、额叶皮层埋置电极,记录氟桂利嗪(20 mg/kg)灌胃后大鼠癫痫样放电的变化.结果:实验组动物皮层及海马癫痫样放电潜伏期明显延长,持续时间缩短,单位时间内癫痫样放电数明显减少,与对照组相比有显著差异.结论:氟桂利嗪具有明显抗癫痫作用,可显著抑制青霉素致痫鼠皮层及海马区癫痫样放电.     

幼年大鼠视皮层神经元对闪光刺激的反应特性

哺乳动物视觉系统的发育延续到出生后,大鼠出生后 3~5 周是视觉系统发育的关键期 . 在关键期中,视皮层的兴奋性和抑制性突触连接逐渐成熟,形成有效的皮层内回路 . 为了观察发育关键期大鼠视皮层神经元的反应特性与成年大鼠的异同,使用胞外单细胞记录的方法对比研究了幼年和成年大鼠对闪光刺激的视觉反应特性 . 结果显示：与成年大鼠相比较,幼年大鼠视皮层神经元对持续闪光刺激显示出更强的适应性,对光刺激的诱发放电频率更低,而在没有光刺激时的自发放电频率更高,从而导致信噪比更低 . 这一结果表明,幼年大鼠视皮层对连续刺激的反应能力下降,对信号的分辨能力也更弱,其原因可能是兴奋性突触和抑制性突触发育的不同步所致 .     

苍白球电毁损对帕金森病大鼠HVSs 振荡波的影响研究

目的:应用直流电核团毁损术毁损帕金森病(PD)大鼠模型的内侧苍白球(GPi),记录其手术前后脑电生理活动的变化,以探讨内苍白球射频毁损术治疗PD的可能机制。方法:成年SD大鼠随机分为GP毁损组、假手术组及正常组。对PD毁损组和假手术组大鼠采用6-羟基多巴胺(6-OHDA)右侧黑质致密部(SNc)、中脑腹侧被盖区(VTA)两点注射法建立PD大鼠模型,并经腹腔注射阿扑吗啡(APO)诱发旋转以对模型建立进行评价。通过多导联宏电极在体脑电生理记录技术对各组大鼠进行右侧(注射侧)大脑皮层M1、M2区脑电及纹状体场电位的连续24小时记录,同时进行视频录像。对GP毁损组大鼠行直流电GPi毁损术,术后4天对各组大鼠均行阿扑吗啡诱导旋转行为检验,继续记录脑电活动,记录数据经频率谱分析及相干分析以揭示各记录位点信号的频率成分以及不同位点神经元集群间的功能连接和同步性。结果:对GP毁损组大鼠毁损术前后在清醒静息状态下的皮层脑电和纹状体场电位有明显改变,术后HVSs(High Voltage Spindles)在持续时间上明显缩短发作次数明显减少;对各组大鼠术后在静息状态下的脑电信号进行对比,GP毁损组大鼠较假手术组的HVSs持续时间和发作频率均减少并接近正常组大鼠水平,相干性分析显示GP毁损组大鼠术后在HVSs频段(5-13Hz)上的相干程度显著小于假手术组。结论:在清醒静息状态下6-OHDA建立的PD大鼠皮层-基底节环路上HVSs持续时间延长发生频率增高,经GP毁损术后其时间缩短发作次数减少同步性降低并接近正常水平,从而改善PD症状,该现象可能解释临床采用苍白球射频毁损术治疗PD的治疗机制。     

一次性力竭运动过程中大鼠“黑质-丘脑-皮层”通路神经元相干性及递质动态变化

目的:通过观察一次性力竭运动过程中大鼠"黑质-丘脑-皮层"通路核团间神经元电活动的相干性及各核团神经递质谷氨酸(Glu)和γ-氨基丁酸(GABA)的浓度,探讨运动疲劳发生过程中大鼠"黑质-丘脑-皮层"通路神经元电活动的可能机制。方法:40只雄性Wistar大鼠,随机分为神经元电活动实时测定组、黑质网状部(SNr)神经元胞外神经递质实时测定组、丘脑腹外侧核(VL)神经元胞外神经递质实时测定组及皮层辅助运动区(SMA)神经元胞外神经递质实时测定组(n=10)。大鼠提供3级递增负荷跑台运动方案进行一次性力竭运动,通过自身对照,观察神经元电活动实时测定组大鼠SNr、VL及SMA神经元细胞在一次性力竭运动前、中、后神经元电活动的动态变化,同步、动态观察神经元胞外神经递质实时测定组大鼠一次性力竭运动前、中、后大鼠SNr、VL及SMA胞外Glu和GABA的浓度及其比值变化。结果:黑质网状部、丘脑腹外侧核局部场电与皮层脑电在力竭运动过程的不同阶段脑区之间神经元电活动,在0~30 Hz范围内均存在显著相干性。与安静状态相比较,自主运动期,大鼠黑质网状部神经元胞外Glu浓度、Glu/GABA比值均显著下降(P0.05,P0.01),GABA浓度则显著升高(P0.05,P0.01),而丘脑腹外侧核及皮层辅助运动区神经元胞外Glu浓度、Glu/GABA比值均显著升高(P0.05,P0.01),GABA浓度则显著下降(P0.05,P0.01);疲劳初期和力竭期,大鼠黑质网状部神经元胞外Glu浓度、Glu/GABA比值均显著升高(P0.05,P0.01),GABA浓度则显著下降(P0.05,P0.01),而丘脑腹外侧核及皮层辅助运动区神经元胞外Glu浓度、Glu/GABA比值均显著下降(P0.05,P0.01),GABA浓度则显著升高(P0.05,P0.01)。结论:大鼠在一次性力竭运动过程中"黑质-丘脑-皮层"通路各核团之间存在神经网络联系,该通路各核团神经递质Glu、GABA浓度的改变是导致其神经元电活动变化的因素之一。     

Neuroprotective effect of mexiletine in the central nervous system of diabetic rats

Both experimental and clinical studies suggests that oxidative stress plays an important role in the pathogenesis of diabetes mellitus type 1 and type 2. Hyperglycaemia leads to free radical generation and causes neural degeneration. In the present study we investigated the possible neuroprotective effect of mexiletine against streptozotocin-induced hyperglycaemia in the rat brain and spinal cord.30 adult male Wistar rats were divided into three groups: control, diabetic, and diabetic-mexiletine treated group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Mexiletine (50 mg/kg) was injected intraperitoneally every day for six weeks. After 6 weeks the brain, brain stem and cervical spinal cord of the rats were removed and the hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for biochemical analysis (the level of Malondialdehide [MDA], Nitric Oxide [NO], Reduced Glutathione [GSH], and Xanthine Oxidase [XO] activity). MDA, XO and NO levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the diabetic group increased significantly, when compared with control and mexiletine groups (P < 0.05). GSH levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the diabetic group decreased significantly when compared with control and mexiletine groups (P < 0.05).This study demonstrates that mexiletine protects the neuronal tissue against the diabetic oxidative damage.     

糖尿病大鼠弓状核-海马肥胖抑素通路构成及对胃运动和胃排空的影响

目的: 探究糖尿病大鼠弓状核(ARC)-海马肥胖抑素(obestatin)神经通路构成,以及该通路对大鼠胃运动、胃排空的影响。方法: 健康雄性Wistar大鼠采用果糖溶液诱导胰岛素抵抗加腹腔注射链脲佐菌素的方法制备糖尿病模型,造模之后,随机分为5组:对照组(NS组)、0.1、1和10 pmol obestatin组、obestatin+NBI27914组,每组7只;各组通过置管分别向海马内注射0.5 μl 生理盐水(NS)、obestatin(0.1 pmol、1 pmol、10 pmol)和混合液(10 pmol obestatin + 60 pmol NBI27914),给药后立即记录大鼠胃运动,15 min后进行胃排空研究;通过荧光金(FG)逆行追踪及免疫组化方法比较正常及糖尿病大鼠ARC-海马obestatin神经通路构及ARC obestatin mRNA表达的异同。结果: 与正常大鼠相比,糖尿病大鼠ARC FG/obestatin双标神经元数目显著减少(P＜0.05),ARC obestatin mRNA表达量显著下降(P＜0.05);obestatin各组可剂量依赖性的抑制大鼠胃运动及胃排空(P＜0.05~0.01),obestatin的这些效应可被促肾上腺皮质激素受体1(CRFR1)阻断剂NBI27914部分阻断(P＜0.05);obestatin对糖尿病大鼠胃运动和胃排空的抑制效应显著减弱(P＜0.05)。结论: ARC-海马之间存在obestatin神经和功能通路,参与糖尿病大鼠胃运动及胃排空调控,且CRFR1信号通路参与该过程。该通路功能的减弱可能参与了糖尿病早期胃动力紊乱的发病。     

Monoamines and self-stimulation of the medial prefrontal cortex in the rat

The participation of noradrenaline (NE) and serotonine (5-HT) in self-stimulation (SS) of the medial prefrontal cortex (MPC) in the rat has been studied. Three groups of rats with bilateral electrodes implanted into the MPC were used in these experiments. In one of the groups, electrodes were also implanted into the locus coeruleus. In the first group, the rats received systemic injections of the following drugs: clonidine (alpha-agonist), phenoxybenzamine (alpha-antagonist), isoproterenol (beta-agonist) and propranolol (beta-antagonist). In the second group, p-chlorophenylalanine (a 5-HT synthesis inhibitor) was administered intragastrically and SS measured during the following 16 days. In these two groups of rats and previous to every SS session, spontaneous motor activity (SM) was measured as control for non specific effects of the drugs. In a third group of rats, lesions of the locus coeruleus were performed unilaterally and SS measured in both prefrontal cortex during the following 16 days post-lesion. SS contralateral to the lesioned side served as control for non-specific effects of the lesions. After all these treatments, SS of the MPC was not specifically affected. Our results suggest the non participation of NE and 5-HT terminals in the neural substrates underlying SS of the MPC.     

Effects of chlorogenic acid,caffeine and coffee on components of the purinergic system of streptozotocin-induced diabetic rats

We evaluated the effect of chlorogenic acid (CGA), caffeine (CA) and coffee (CF) on components of the purinergic system from the cerebral cortex and platelets of streptozotocin-induced diabetic rats. Animals were divided into eight groups: control animals treated with (I) water (WT), (II) CGA (5 mg/kg), (III) CA (15 mg/kg) and (IV) CF (0.5 g/kg), and diabetic animals treated with (V) WT, (VI) CGA (5 mg/kg), (VII) CA (15 mg/kg) and (VIII) CF (0.5 g/kg). Our results showed an increase (173%) in adenosine monophosphate (AMP) hydrolysis in the cerebral cortex of diabetic rats. In addition, CF treatment increased adenosine diphosphate (ADP) and AMP hydrolysis in group VIII synaptosomes. Platelets showed an increase in ectonucleotidase activity in group V, and all treatments reduced the increase in adenosine triphosphate and ADP hydrolysis. Furthermore, there was an increase in platelet aggregation of 72% in the diabetic rats, and CGA and CF treatment reduced platelet aggregation by nearly 60% when compared to diabetic rats. In this context, we can suggest that CGA and CF treatment should be considered a therapeutic and scientific target to be investigated in diseases associated with hyperglycemia.     

妊娠合并糖尿病诱发胚胎先天性神经管缺陷 动物模型的MAP 激酶信号传导机制MAP

为了揭示妊娠合并糖尿病诱发胚胎先天性神经管缺陷的分子机制,并探讨其有效的防治方法。 实验选用6个实验组的 Sprague-Dawley 大鼠：第1组为常规饲养的正常对照组;第2组尾静脉注射65mg/kg Streptozotocin (STZ) 构建妊娠合并糖尿病、且诱发先天性神经管缺陷的实验组大鼠;第3组为STZ构建的糖尿病、但胚胎不伴有先天性神经管缺陷的大鼠模型;第4、5、6 组为 STZ 构建的糖尿病治疗组大鼠,每日分别给予80mg/mL花生四烯酸 (arachidonic acid,AA)、400mg 维生素E、抗氧化剂(维生素 E) 和不饱和脂肪酸 (saflower oil) 混合物 cocktail 治疗。于妊娠第12天取出各组胚胎,解剖显微镜下进行形态学分析;提取卵黄囊细胞蛋白质,应用特异性抗磷酸化抗体进行免疫共沉淀及 Western 印迹,对MAP 激酶 信号途径上各蛋白激酶ERK1/2、JNK1/2、RAF-1活性进行分析。 与正常对照组相比,妊娠合并糖尿病诱发的先天性神经管缺陷胚胎中(第2组),ERK1/2蛋白激酶活性显著下降,其上游 RAF-1活性相应降低;与此相反,JNK1/2活性明显升高。在给予花生四烯酸、维生素E 补充物治疗后,通过调节MAP 激酶 信号通路蛋白激酶活性,逆转了胚胎神经管缺陷的发生。妊娠合并糖尿病诱发的胚胎先天性神经管缺陷的发生,与MAP 激酶信号传导机制异常密切相关。不饱和脂肪酸和抗氧化剂补充物的治疗作用通过对MAP 激酶信号途径的调控实现的。 AbstractThe aim of the present study was to determine molecular mechanism in hyperglycemia-induced congenital neural tube defects and the its potential pharmacologic rescuing agents. In order to explore these questions, six study groups of Sprague-Dawley rats were employed: Group 1 was normal control rats with normal diet; group 2 represented streptozotocin (STZ) -induced diabetic rats with congenital neural tube defects in offspring; group 3 included STZ-induced diabetic rats with normal offspring; groups 4,5 and 6 included rats exposed to the same STZ-induced diabetic condition, but receiving daily oral supplementation of 80mg/mL of the sodium salt of arachidonic acid (AA), 400mg of vitamin E and a cocktail of a polyunsaturated fatty acid (saflower oil) plus an antioxidant ( vitamin E) respectively. Yolk sac cells were harvested at gestational day 12 from each rat group. Changes in MAPK signaling pathways were detected by western blot analysis using special antibodies directed against phosphorylated forms of extracellular signal regulated kinase (ERK), Jun N-terminal/stress-activated protein kinase (JNK/SAPK). Furthermore, activity of RAF-1, an upstream kinase in ERK1/2 signaling cascade, was evaluated by immunoprecipitation assay. The results showed that in yolk sac cells in embryopathic offspring from experimentally-induced diabetic rats, activities of ERK1/2 were dramatically decreased (group 2). Consisted with these observation, reduction in RAF-1 kinase activity could be discerned in these diabetic yolk sac cells. In contrast, activities of JNK1/2 were significantly increased in yolk sac cells of group 2. Under rescuing circumstance,activations of ERK1/2 and RAF-1 were increased, and JNK1/2 were decreased. MAP kinase signal pathway plays a very important role in hyperglycemia induced neural tube defects. The supplementation of polyunsaturated fatty acid arachidonic acid, and antioxident vitamin E rescued conceptuses from diabetic embryopathy by triggering a restoration of normal membrane signaling pathways.     

Increased RhoA translocation in renal cortex of diabetic rats

RhoA, a member of the Rho small G protein family, mediates multiple intracellular signaling pathways, and is highly expressed in renal cortex. RhoA translocation is associated with RhoA activation. This study was undertaken to examine the relation of translocation of RhoA in the renal cortex with diabetic renal injury in streptozotocin (STZ)-induced diabetic rats. Male Sprague-Dawley rats were divided into control and diabetic groups and were studied at 8 weeks after STZ-injection (55 mg/kg, i.v). We found that the kidney weight and urinary protein excretion were significantly increased in diabetic rats. Diabetic glomerulopathy was confirmed by mesangial matrix expanding and glomerular basement membrane thickening. The ratio of membrane-bound RhoA verses cytosolic RhoA is 1.8 fold higher (p < 0.01) in diabetic group, indicating an enhanced RhoA translocation. There was no significant difference in total RhoA protein expression and RhoA mRNA expression between diabetic and control groups. These data suggest that RhoA translocation might be involved in diabetic renal injury.     

金樱子提取液对糖尿病肾病大鼠的肾脏保护作用

目的:研究金樱子提取液对糖尿病肾病(Diabetic Nephropathy,DN)大鼠的肾脏保护作用。方法:在高糖高脂饲料喂食SD(Sprague-Dawley)大白鼠的基础上腹腔注射链脲佐菌素(streptozotocin,STZ)诱导糖尿病肾病大鼠模型,随机分为糖尿病肾病模型组(DN组)和金樱子治疗组(DN+RLM组),同时另设正常对照组(NC组)和金樱子对照组(NC+RLM组)。检测金樱子提取液对各组大鼠血糖(fasting blood-glucose,FBG)、糖化血红蛋白(glycosylated haemoglobin,GHb)、24小时尿微量白蛋白和尿量、血尿素氮(BUN)、血肌酐(Scr)、胆固醇(TC)、甘油三酯(TG)及肾脏结构的影响。结果:与DN大鼠相比,糖尿病肾病大鼠经金樱子提取液治疗后,大鼠FBG、GHb水平、24 h尿微量白蛋白、24 h尿量、肾脏指数明显降低,血脂紊乱、肾功能损害以及DN肾脏病理明显改善,且无明显副作用。结论:金樱子提取液可明显降低DN大鼠血糖,改善DN大鼠血脂、肾功能紊乱及肾脏病理变化,对糖尿病大鼠肾脏具有较强的保护作用。     

电针足三里穴对糖尿病胃轻瘫大鼠延髓多巴胺能神经元和 星形胶质细胞活性的影响

目的:研究电针足三里穴对糖尿病胃轻瘫大鼠延髓多巴胺能神经元内酪氨酸羟化酶(tyrosine hydroxylase,TH)和星形胶质细胞内胶质原纤维酸性蛋白(Glial Fibrillary Acidic Protein,GFAP)表达的影响。方法:32只实验大鼠分为空白对照(空白)组、糖尿病胃轻瘫模型(模型)组、模型组+电针足三里穴(足三里)组和模型组+电针非经非穴(非经非穴)组(每组8只)。模型制备采用腹腔注射5%四氧嘧啶和熟地灌胃诱导的方法。实验3周后取大鼠延髓进行抗TH和抗GFAP的单一和双重免疫组化染色,观察并记数TH和GFAP在延髓内的表达。结果:与空白组比较,各实验组TH阳性多巴胺能神经元和GFAP阳性星形胶质细胞集中表达于延髓迷走孤束复合体内,有明显的定位特点;高倍镜下观察到TH阳性神经元周围有大量GFAP阳性星形胶质细胞包绕。各组TH和GFAP表达以模型组最高;而足三里组TH阳性多巴胺能神经元数量明显减少(31.3±4.4→16.8±3.2),GFAP阳性产物表达明显降低(113.8±7.6→95.4±8.4),且它们之间有统计学意义(P<0.01);非经非穴组与模型组之间差异没有统计学意义。结论:针刺调节糖尿病胃运动功能障碍大鼠与其调控延髓多巴胺能神经元及其周围的星形胶质细胞功能活动有关。     

早期糖尿病肾病大鼠模型磁共振弥散加权成像的初步研究

目的:探讨早期糖尿病肾病(Diabetic nephropathy,DN)模型大鼠磁共振弥散加权成像(Diffusion Weight Imaging,DWI)肾实质ADC值变化规律。方法:将20只清洁级雄性SD大鼠随机分成两组,糖尿病肾病组(DN组)12只,正常对照组(NC组)8只;DN组给予60 mg/kg链尿佐菌素腹腔注射诱导糖尿病肾病模型,NC组按照相同方法、相同剂量柠檬酸缓冲液腹腔注射;并对最终糖尿病模型造模成功并且存活的8只DN大鼠、8只NC大鼠进行MRI扫描,包括常规轴位T1WI、T2WI扫描及DWI扫描;扫描结束后收集血液送血肌酐及双肾组织进行病理检查。并测量每只大鼠双肾皮、髓质的ADC值。结果:造模后,DN组大鼠血糖明显升高、尿量明显增加、体重明显减低,DN组大鼠肾脏出现不同程度病理损伤,符合早期DN病理改变。DN组大鼠肾脏皮、髓质ADC值分别为1.522±0.913×10^-3 mm^2/s、1.268±0.388×10^-3 mm^2/s,较NC组肾脏皮、髓质ADC值1.276±0.341×10^-3 mm^2/s、1.011±0.217×10^-3 mm^2/s增高,两组比较有统计学意义(P<0.05)。结论:DWI成像ADC值可能反映早期糖尿病肾病肾脏功能的变化。