锌对妊娠大鼠汞暴露后胎鼠脑损伤的保护作用

锌足人体必需的微量元素之一,母体可通过金属硫蛋白的转运、离子扩散等方式将锌转运给胎儿[1]。研究已证实锌不但为胚胎发育所必需,且在胚胎发育中可能有更重要的作用。汞是生命非必需元素,国内外研究证实汞可以通过胎盘屏障,对发育中胎儿产生毒性作用,其靶器官主要足脑[2]。目前对汞中毒的治疗没有理想方法,尤其是孕期汞中毒的治疗。汞毒性的发生机制足复杂多方面的,其中促进细胞凋亡、抑制抗过氧化物酶体系的活性,导致膜脂和膜蛋白损伤是主要机制。本研究拟通过建立动物模型,探讨孕期补锌对染汞孕鼠胎鼠脑损害的保护作用及其作用机制。     

母源性BDE-209胃灌后对子鼠学习记忆能力的影响以及血清BDE-209浓度的测定

目的研究母鼠在妊娠期及哺乳期接触十溴联苯醚(brominated diphenyl ethers-209,BDE-209)对子鼠的学习记忆能力的影响以及血清BDE-209的浓度测定。方法通过胃灌的方法造成Wistar大鼠BDE-209[300mg/(kg.d)]的暴露模型,直至生育出的子鼠断乳,通过Y型迷宫测试子鼠的学习记忆能力。然后分别取母鼠及子鼠的血清进行BDE-209的测定。结果终生胃灌BDE-209组的大鼠学习能力为89.65±6.68,记忆能力为平均为4.75±1.25,均较对照组(学习能力68.85±9.28,记忆能力8.05±0.76)有明显的下降,差异有统计学意义(P<0.01);妊娠期以及哺乳期均胃灌组学习能力为74.40±8.26,较正常对照组有下降,差异有统计学意义(P<0.05),但记忆能力下降差异无统计学意义(P>0.05);单纯哺乳期胃灌组较对照组学习记忆能力下降差异无统计学意义(P>0.05);母鼠血清中BDE-209的含量与子鼠正相关。结论BDE-209可以通过胎盘屏障以及母乳进入胎鼠体内并有一定程度的蓄积,并且可以影响发育中的子鼠神经系统,降低子鼠的学习记忆能力检测。     

沙棘总黄酮对新生大鼠缺氧缺血性脑损伤的保护作用

新生儿缺氧缺血性脑病（hypoxic-ischemic encephalopathy，HIE）是新生儿常见疾病，致死、致残率较高。现代药理学研究表明沙棘总黄酮具有阻滞钙离子内流、清除自由基、抗生物膜过氧化等作用。因此，本研究以新生大鼠缺氧缺血性脑病模型，观察沙棘总黄酮对神经细胞的保护作用。     

早期干预改善宫内缺氧缺血性脑损伤新生大鼠学习记忆能力的效果评价

新生儿缺氧缺血性脑病(HIE)发病率高，常导致智能迟缓等严重后遗症。对急性期发生的脑损伤尚缺乏有效的治疗方法。有研究发现早期干预可改善宫内缺氧缺血性脑损伤(HIBD)新生大鼠的脑功能。本研究对宫内HIBD干预组及正常干预组新生大鼠进行早期干预28d，通过“Y”臂迷宫检测学习分辨能力、记忆保持百分率判断干预效果，并观察额皮质和海马CA2区、     

细胞红蛋白对新生大鼠缺氧缺血性脑损伤的神经保护作用

目的 探讨细胞红蛋白(cytoglobin,CYGB)在缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)中的神经保护作用. 方法 健康7日龄新生Sprague-Dawlay大鼠随机分为假手术组、HIBD组、HIBD+氯化高铁血红素(Hemin)组和HIBD+锌原卟啉(zinc protoporphyrin,ZnPP)组.HIBD组、HIBD+ Hemin组及HIBD+ ZnPP组大鼠分别腹腔注射0.5 ml生理盐水、Hemin(50 mg/kg)及ZnPP(50 mg/kg),12h后结扎并剪断左侧颈总动脉,缺氧2h,制成HIBD动物模型.建立模型后0、24、48 h免疫组织化学法检测各组大鼠海马及皮质中CYGB的表达情况,每组10只.HE染色观察建立模型后48 h的大鼠脑组织病理变化,每组8只.称重法检测建立模型后72h新生大鼠脑含水量,每组8只.建立模型后28 d采用Morris水迷宫实验检测海马学习记忆功能变化,每组10只.组间差异比较采用方差分析,组间两两比较使用Bonferroni法. 结果 (1)大鼠脑组织CYGB的表达水平:用平均灰度值(与蛋白表达水平成反比)表示.在0h,HIBD+ Hemin组和HIBD组皮质CYGB的平均灰度值分别为166.7±5.1和207.1±5.1,低于假手术组(232.3±3.4),而HIBD+ ZnPP组(234.9±4.5)高于假手术组(P＜0.05).随时间的增加,各HIBD组CYGB的平均灰度值递减,至48 h时,CYGB的平均灰度值HIBD+Hemin组最低(126.0±2.6),其次是HIBD组(150.9±4.5)和HIBD+ ZnPP组(163.7=6.3),最高是假手术组(232.1±5.8),差异均有统计学意义(P均＜0.01).CYGB在海马组织的表达变化与皮质一致.(2)各组脑组织病理变化:建立模型后48 h,HIBD组、HIBD+ Hemin组和HIBD+ ZnPP组新生大鼠脑组织可见典型的脑梗死和出血,HIBD+Hemin组梗死灶明显较HIBD+ZnPP组小,出血减轻.(3)脑组织含水量变化:建立模型后72 h,HIBD组和HIBD+ZnPP组左侧脑组织含水量分别为(86.5±0.4)％和(87.3±0.3)％,明显高于右脑[(85.6±0.2)％和(85.9±0.2)％],差异有统计学意义(t分别为12.57和11.32,P均＜0.01).(4)海马学习记忆功能变化:水迷宫实验中,5d总平均逃逸潜伏期HIBD+ ZnPP组最长[(76.7±29.8)s],其次是HIBD组[(71.0±30.5)s]和HIBD+ Hemin组[(46.7±34.0)s],最短为假手术组[(38.3±30.3)s],差异均有统计学意义(P均＜0.05).(5)远期脑组织病理变化:建立模型后34 d,脑组织萎缩率HIBD+ ZnPP组最高[(34.07±6.75)％],其次是HIBD组[(29.73±6.53)％],再次是HIBD+Hemin组[(18.33±4.52)％],均高于假手术组[(1.55±1.32)％],差异均有统计学意义(P均＜0.01).HIBD组及HIBD+ZnPP组大鼠脑组织可见锥体细胞层变薄,大片神经元缺失,HIBD+Hemin组仅见少量神经元缺失. 结论 CYGB的高表达可减轻HIBD脑组织近期及远期的病理损伤,保护远期的海马学习记忆功能.     

外源性神经节甘脂对缺氧缺血性脑损伤新生鼠学习记忆的增强作用

目的　探讨外源性神经节甘脂 (gangliosides,GAs)对缺氧缺血性脑损伤 (hypoxic- is-chem ic brain damage,HIBD)新生大鼠学习记忆能力的影响。　方法　选用 7日龄 SD大鼠 ,结扎右侧颈总动脉 ,吸入氧浓度为 8%的氮氧混合气体 ,制作新生大鼠 HIBD模型。制模后的大鼠随机分为三组 :实验组 1,神经节甘脂 5 0 mg/ kg,腹腔注射 ,12 h 1次 ,共 4次 ,以后 30 mg/ (kg· d) ,连续注射 2周 ,(简称 GAs× 2周组 ) ;实验组 2 ,神经节甘脂 5 0 mg/ kg,腹腔注射 ,12 h 1次 ,共 4次 ,以后注射等量生理盐水 2周 ,(简称 GAs NS组 ) ;对照组 ,注射等量的生理盐水。采用三等分迷宫检测大鼠的分辨学习能力和记忆保存能力 ,并观察大鼠的活动状态和交互行为 (此时大鼠日龄为 2 4d)。最后进行脑组织病理检查。　结果　 (1)大鼠达到学会标准所需的训练次数 :对照组 (39± 17)次 ,GAs NS组 (32±14)次 ,GAs× 2周组 (2 0± 13)次 ;记忆保存能力测试结果为 :对照组 (6 2± 10 ) % ,GAs NS组(6 4± 11) % ,GAs× 2周组 (70± 9) %。 GAs× 2周组大鼠的学习记忆能力好于 GAs NS组和对照组(P<0 .0 1,P<0 .0 5 )。 (2 ) GAs× 2周组在三臂迷宫中的活动较对照组和 GAs NS组少。 (3)实验组和对照组交互行为差异无显著性 ;(4)三组大鼠海马     

早期高压氧对缺血缺氧性脑损伤新生大鼠脑神经保护的效果探讨

目的探讨早期高压氧对缺血缺氧性脑损伤(HIBD)新生大鼠脑神经保护的效果。方法将7日龄新生Wistar大鼠120只随机分为假手术组、HIBD组、高压氧组,每组各40只。将高压氧组再随机分为早期高压氧亚组和晚期高压氧亚组,每亚组各20只。对所有大鼠建立HIBD模型后(假手术组采用假手术处理),早期高压氧亚组在建模后1h内,晚期高压氧亚组在建模后48h实行高压氧治疗(2ATA,每次90min,24h1次,连续治疗7d)。各亚组治疗结束后处死大鼠,假手术组与HIBD组处死等量大鼠。利用免疫组织化学法对大鼠海马中神经巢蛋白(Nestin)的含量进行检测,利用Morris水迷宫实验对大鼠学习记忆功能进行检测。结果假手术组Nestin阳性细胞检出数量为(10.26±1.37)个/HP,早期高压氧亚组Nestin阳性细胞检出数量为(15.82±2.19)个/HP,晚期高压氧亚组Nestin阳性细胞检出数量为(32.64±4.83)个/HP,HIBD组Nestin阳性细胞检出数量为(36.18±4.02)个/HP。高压氧组和HIBD组Nestin阳性细胞检出数量显著高于假手术组,差异有统计学意义(P0.05),晚期高压氧亚组显著高于早期高压氧亚组,差异有统计学意义(P0.05),晚期高压氧亚组与HIBD组比较,差异无统计学意义(P0.05);4组平均逃逸潜伏期差异有统计学意义(F=24.18,P0.05),假手术组早期高压氧组晚期高压氧组HIBD组;假手术组、早期高压氧组和晚期高压氧组3组大鼠在搜索耗时和搜索路程上组间比较,差异有统计学意义(F=21.05,P0.05),假手术组早期高压氧组晚期高压氧组,而晚期高压氧组和HIBD组组间比较差异无统计学意义(P0.05),各组搜索速度组间比较,差异无统计学意义(P0.05)。结论早期高压氧对HIBD脑损伤具有保护功能,Nestin蛋白可能参与了脑神经的修复过程,早期高压氧还对HIBD引起的远期学习记忆功能障碍有改善作用。     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

目的 观察缺氧缺血(HI)对3日龄大鼠脑细胞凋亡及成年后头部MRI影像和学习记忆能力的影响.方法 应用凋亡基因芯片研究3日龄大鼠缺氧缺血性脑损伤后12 h与损伤7 d凋亡基因表达的差异.42日龄时进行大脑MRI检查,并在44日龄时采用水迷宫测试其学习和记忆能力.组间比较采用t检验和秩和检验.结果 与HI脑损伤后12 h相比,损伤后7 d表达上调的基因包括TNF及其受体家族中的Tnfsf10(TRAIL)、Tnfsf13(CD30)、Tnfrsf21、Tnfrsf11b;Caspase家族中的Caspase1、2、3和6;Bcl2家族中的促凋亡基因Bak1、Becn1、Bcl10和Bid3;死亡域TRADD和Myd88.而Caspase 8和抗凋亡基因Mapk8ip表达下调.42日龄时头部MRI检查显示HI组右侧大脑皮质面积较左侧和假手术组显著减小[侧脑室层(23.5±3.6)mm2、(33.0±4.3)mm2和(34.5±3.9)mm2(F=17.09,P<0.01);海马层(18.9±4.4)mm2、(29.1±5.0)mm2和(30.8±4.5)mm2(F=14.44,P<0.01)].HI组水迷宫试验上台时间在第4天为(52.7±35.9)s,明显长于假手术组的(17.8±8.9)s(P<0.01).记忆测试中,HI组大鼠经过站台的次数显著少于假手术组(T=292.5,P<0.05).结论 3日龄SD大鼠HI脑损伤后,神经细胞凋亡基因激活持续到损伤后7 d,涉及凋亡的外源性和内源性通路.神经细胞的凋亡会导致大脑皮层萎缩,可能影响动物成年后的空间学习和记忆能力.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响

Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.     

亚低温对缺氧缺血脑损伤保护作用的实验研究

目的 探讨新生鼠缺氧缺血脑损伤后实施亚低温的最佳疗程和温度.方法 实验性缺氧缺血脑损伤模型鼠(n=82)于损伤后分为三组:室温恢复组(n=22)由母鼠喂养;环境温度29℃或31℃两组动物(n=60)分别进行24小时、48小时和72小时的亚低温干预,此期间采用配方奶喂养,干预结束后仍由母鼠喂养,观察血糖、血气和病理变化以判断疗效.结果 环境温度31℃或29℃可降低脑温3℃或5℃.血糖维持正常,病理结果发现亚低温干预可使脑损伤程度减少46%～86%.结论 缺氧缺血后连续72小时降低脑温4～5℃能取得最佳的脑保护作用.     

对新生鼠缺氧缺血性脑损伤的几种保护作用的研究

目的　研究脑活素 (L ZCL )、胞二磷胆碱 (CDPC)及碱性成纤维细胞生长因子 (b FGF)对新生大鼠缺氧缺血性脑损伤 (HIBD)的保护作用。　方法　应用新生 Wistar大鼠制备 HIBD模型 ,将 L ZCL、CDPC和 b FGF应用于这些模型中 ,观察它们对 HIBD模型鼠的体重增长、病死率、脑病变的影响 ,并用原位缺口末端标记法检测它们对缺氧缺血 (HI)后脑细胞凋亡的影响。　结果　 3种治疗均促进了 HIBD模型鼠体重的增长 ,明显减轻了脑水肿及脑病变 ,并减轻了 HI后脑细胞的凋亡。　结论　 L ZCL、CDPC及 b FGF对 HIBD的脑组织确有保护作用。