老年腔隙性脑梗死患者抑郁情绪及影响因素的研究

脑梗死后抑郁状态是脑卒中常见的并发症之一 ,其发生率为 2 3%～ 6 5 % [1] 。脑梗死后抑郁不仅严重影响患者的生活质量 ,而且可直接影响其康复和预后。随着医学影像学的发展 ,腔隙性脑梗死(Ｌａｃｕｎａｒｃｅｒｅｂｒａｌｉｎｆａｒｃｔｉｏｎ ,ＬＩ)的诊断率逐渐增高。为探讨老年ＬＩ患者抑郁的临床特点 ,我们收集老年ＬＩ病人 12 6例 ,对其抑郁的特点、抑郁症状与ＬＩ的关系及影响因素进行了研究 ,现报告如下。1　资料与方法1.1　研究对象为 1998年 1月至 2 0 0 0年 12月在本院及济宁市一院精神科住院的ＬＩ病人 12 6例 ,年龄 6 0～ 82…     

Maternal immunity to insulin does not affect diabetes risk in progeny of non obese diabetic mice

It has been suggested that maternal environment, in particular maternal autoantibodies, modify the risk of developing autoimmune diabetes in offspring. The aim of this study was to determine whether modification of maternal environment and maternal diabetes risk through immunization affects autoimmune diabetes risk in the progeny. The risk of developing insulin antibodies and of developing diabetes was determined in 113 female progeny of non obese diabetic (NOD) dams that were immunized with insulin, control antigen or vehicle before or during pregnancy. Although NOD dams immunized with insulin were rendered diabetes resistant (40% diabetes by age 36 weeks versus 100% in control dams), diabetes development in their female offspring (72%, 26/36) was similar to that in female offspring of dams immunized with glucagon (82%, 22/27) or vehicle (76%, 19/25). Furthermore, no significant differences in diabetes development or insulin autoantibody titres were observed between female progeny of insulin autoantibody positive NOD dams (82% diabetes by age 36 weeks, 18/22), insulin autoantibody negative NOD dams (75%, 41/55), and NOD dams that had antibodies against exogneous insulin (71%, 22/31). The findings suggest that modification of the maternal risk for autoimmune diabetes via antigen-specific immunization is not transferred to progeny and that fetal exposure to insulin autoantibodies does not increase the risk for diabetes development.     

联合应用神经保护剂抑制大鼠局灶性脑缺血后的神经元凋亡

目的探讨联合应用神经保护剂能否较单一用药更好地达到保护脑的作用。方法采用线栓法制作大鼠大脑中动脉闭塞模型(MCAO),分为对照组、1,6-二磷酸果糖(FDP)组、MK-801组、N-乙酰半胱氨酸(NAC)组、联合治疗组和假手术组。应用TUNEL染色检测神经元凋亡,免疫组化及W estern b lot检测caspase-3蛋白表达。结果缺血后6 h和24 h,联合治疗组神经元凋亡和caspase-3蛋白表达均明显少于各单一用药组(P<0.05)。结论联合应用神经保护剂对大鼠局灶性脑缺血的保护作用明显增强。     

NGF和CGRP对局灶性脑缺血再灌注后大鼠皮质CHOP蛋白表达的影响

目的探讨外源性神经生长因子(NGF)和降钙素基因相关肽(CGRP)对局灶性脑缺血再灌注后大鼠顶叶皮质神经元CHOP蛋白表达的影响及其作用机制。方法用线栓法制备大鼠大脑中动脉阻塞(MCAO)模型,应用免疫组织化学方法,免疫印迹法(W estern B lotting)测定CHOP蛋白表达;M etamoph图像分析系统对结果进行分析。结果假手术组大鼠顶叶皮质未见CHOP蛋白表达;缺血组CHOP蛋白在缺血再灌注后12 h明显表达,24 h达高峰,72 h显著下降,缺血组较假手术组CHOP蛋白表达显著增加(P<0.01);NGF组和CGRP组CHOP蛋白表达分别弱于缺血组(P<0.01);NGF和CGRP合用组CHOP蛋白表达明显弱于缺血组(P<0.01),也分别弱于NGF组和CGRP组(P<0.01)。结论NGF和CGRP能分别下调局灶性脑缺血再灌注大鼠顶叶皮质CHOP蛋白表达,联合应用则作用更强,二者对保护脑缺血神经元可能有协同作用。     

局灶性脑缺血大鼠皮质和尾壳核神经干细胞增殖分化与nNOS的表达

本研究旨在探讨局灶性脑缺血再灌注大鼠皮质和尾壳核神经干细胞的增殖分化与nNOS表达的关系。大脑中动脉线栓法制作大鼠局灶性脑缺血再灌注模型,5溴脱氧尿核苷(BrdU)标记分裂增殖细胞,免疫组化单标和双标记技术检测各组大鼠缺血侧皮质和尾壳核BrdU阳性细胞和nNOS的表达。模型组大鼠皮质和尾壳核BrdU阳性细胞再灌注后3d开始增多,14d达高峰,nNOS阳性细胞再灌注后7d表达增强,28d达高峰,BrdU/nNOS双标细胞在14d达高峰,占皮质BrdU阳性细胞数的42.95%,尾壳核内占42.56%。新生细胞分化组BrdU阳性细胞和BrdU/nNOS双标细胞显著多于模型组(P<0.05),皮质双标细胞占BrdU阳性细胞数的54.08%,尾壳核内占47.84%。提示局灶性脑缺血可增强大鼠皮质和尾壳核的增殖能力,部分增殖细胞分化为nNOS阳性神经元,参与神经网络的重建。     

人参皂甙Rb1阻止大鼠局灶性脑缺血细胞凋亡和诱导NAIP表达(英文)

人参皂甙Rb1(GRb1)是人参中一个最重要的有效成分(人参属五加科中一属),能减少大鼠暂时性脑缺血梗塞面积和改善神经功能缺失症状,这种神经保护作用的机制不完全清楚。本实验研究GRb1的神经保护作用是否与防止神经元凋亡和调控神经元凋亡抑制蛋白(NAIP)的表达有关。通过阻塞大鼠大脑中动脉建立局灶性脑缺血模型,再灌注开始后立即给予腹腔注射GRb1(40mg/kg)。具有神经功能缺失的大鼠被随机分成2组:缺血组和GRb1组,每个组根据再灌注时间(3h,12h,1d,2d,3d,5d,10d,n=4/每时间点)分为亚组。正常大鼠和假手术组做为对照组。TUNEL标记分析凋亡细胞,用免疫组织化学的方法检测NAIP的表达。结果显示再灌注3h凋亡细胞数量开始升高,24h达高峰,后下降,但再灌注10d的凋亡细胞数量显著高于对照组(P<0.01)。与缺血组相比,GRb1各亚组的凋亡细胞数减少,但再灌注12h至3d,其差异具有统计学意义。在对照组,NAIP弱或阴性的免疫反应广泛出现在脑实质神经元。再灌注3h,NAIP阳性细胞增加,12h时达高峰,后下降。再灌注5d,NAIP阳性细胞数量比对照组少(P<0.05)。NAIP阳性神经元出现缺血性改变如扇形或三角形,纹状体星形胶质细胞强表达NAIP。在GRb1组,NAIP阳性细胞数量从再灌注12h到10d,显著高于缺血组。本实验结果提示大鼠局灶性脑缺血时,GRb1能减少细胞凋亡,其机制可能与增加NAIP的表达有关。     

电针对脑梗塞大鼠缺血半影区星形胶质细胞形态的影响

目的： 观察电针对脑梗塞大鼠缺血半影区星形胶质细胞形态学的影响，为探讨针刺治病疗效和机制提供实验依据。方法： 线栓法建立大鼠脑梗塞动物模型，用免疫组织化学方法显示胶质纤维酸性蛋白（GFAP）免疫阳性细胞，对比观察电针对模型大鼠脑皮质缺血半影区星形胶质细胞的形态影响。结果： 免疫组织化学方法显示电针对脑梗塞缺血半影区星形胶质细胞的数量、细胞面积比与对照组相比差异无显著意义。结论： 频率5-10 Hz和强度2 mA的电针穴位刺激没有影响缺血半影区内星形胶质细胞的形态,但是对GFAP的表达有上调的影响。     

泛素蛋白酶系统在四氧嘧啶诱导的糖尿病大鼠视网膜中的表达

目的:建立泛素蛋白酶系统(UPS)在正常和8周糖尿病大鼠视网膜的表达图谱,探讨其在糖尿病视网膜病变(DR)发生发展中可能的分子机制。方法:在限制片段差异显示PCR(RFDD-PCR)技术建立正常和8周糖尿病大鼠视网膜基因表达谱的基础上,对差异片段进行生物信息学分析,筛选UPS DR相关基因,并以免疫组织化学、半定量RT-PCR技术进行验证。结果:RFDD-PCR结果显示,泛素蛋白酶系统DR相关基因UBS3A、PSMD8和PSMD11在糖尿病组表达上调。RT-PCR结果显示,糖尿病组UBS3A表达比正常组明显增高,PSMD8和PSMD11则仅在糖尿病组中表达。免疫组织化学结果显示,正常组UBE3A阳性免疫反应物见于内丛状层,外丛状层和锥、杆体细胞层,PSMD8和PSMD11未见阳性细胞;糖尿病组UBE3A、PSMD8和PSMD11阳性细胞明显增多,见于节细胞层、内核层和外核层。结论:UPS与DR发生发展有关。     

miR-30a-3p靶向NOD1对心肌细胞缺氧复氧损伤的影响

目的　探究miR-30a-3p与NOD1的靶向关系，及其对心肌细胞缺氧复氧损伤的影响和机制。 方法　将细胞分为Ctrl组、H/R组、miR-30a-3p mimic组和miR-30a-3p inhibitor组，经过缺氧复氧处理后，转染相应的miRNA处理细胞，RT-PCR检测miR-30a-3p和NOD1基因表达水平，荧光素酶报告检测miR-30a-3p和NOD1靶向关系，Western blot检测NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平，CCK8法检测细胞活性，Hoechst检测细胞凋亡，试剂盒检测LDH、CK、MDA、T-SOD水平。 结果　miR-30a-3p表达水平随缺氧复氧处理时间增长而下降，NOD1基因表达水平随缺氧复氧处理时间增长而升高。在荧光素酶报告实验中，NOD1 WT+miR-30a-3p mimic荧光素酶活性显著低于NOD1 WT+NC组。与Ctrl组比较，H/R组miR-30a-3p基因表达水平、细胞活性、T-SOD水平降低，NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平、LDH、CK、MDA水平、细胞凋亡率升高；与H/R组比较，miR-30a-3p mimic组miR-30a-3p基因表达水平、细胞活性、T-SOD水平升高，NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平、LDH、CK、MDA水平、细胞凋亡率降低，miR-30a-3p inhibitor组miR-30a-3p基因表达水平、细胞活性、T-SOD水平降低，NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平、LDH、CK、MDA水平、细胞凋亡率升高。 结论　miR-30a-3p可靶向作用于NOD1，缓解心肌细胞缺氧复氧造成的损伤，其作用机制可能与调控NF-κB信号通路有关。     

The acute effects of insulin on the cardiorespiratory responses to hypoxia in streptozotocin‐induced diabetic rats

Aims: We examined whether or not streptozotocin (STZ)‐induced diabetic rats, which have a lower heart rate (HR, beats min^?1) than control rats, could maintain hypoxic ventilatory response. Methods: Twenty‐six Wistar rats, which had been injected with STZ (60 mg kg^?1, EXP) or vehicle (0.1 m citrate buffer, CONT) intraperitoneally at 9 weeks of age, had their cardiorespiratory responses to normoxia and 12%O₂ examined after 5 weeks. Results: Compared with CONT rats, EXP rats had a higher blood glucose [24 ± 3 vs. 5 ± 1 (mean ± SD) mmol L^?1], a lower body weight (320 ± 23 vs. 432 ± 24 g), lower HR (303 ± 49 vs. 380 ± 44 in normoxia, and 343 ± 56 vs. 443 ± 60 in hypoxia) and a lower mean arterial blood pressure (MAP) (89 ± 6 vs. 102 ± 10 mmHg in hypoxia). In contrast, both groups had similar values in ventilation (), –metabolic rate (MR) ratio and arterial blood gases (ABGs). In EXP rats, with an acute insulin supplement (i.v., 0.75 U h^?1 for 1.5–2 h), not only blood glucose, but also HR, and MAP were normalized as those obtained in CONT rats, and in hypoxia further increased without affecting –MR ratio and ABGs. Such acute cardiorespiratory stimulating effects of insulin could not be obtained in non‐diabetic rats (n = 7, 355 ± 24 g), in which euglycaemia (mean 6.4 mmol L^?1) was maintained during the measurements. Conclusions: Our results suggest that, in STZ‐induced diabetic rats: (1) ventilation is hardly suppressed by hyperglycaemia, (2) cardiorespiratory responses can be acutely stimulated by short insulin injection, and (3) the effects, including those through acute blood glucose normalization, are possibly specific for the diabetic impairments.