新生大鼠缺氧缺血性脑损伤神经细胞凋亡时程

为确定新生大鼠缺氧缺血性脑损伤神经细胞凋亡时程、采用HE染色及TUNEL研究新生大鼠缺氧缺血性脑损伤后神经细胞凋亡情况.结果显示,新生大鼠缺氧缺血后3周时,左脑仍有少量凋亡细胞存在,与对照组比较有显著性差异,P＜0.05;于4周时左脑凋亡细胞数与对照组比较无显著性差异,P＞0.05.结果提示新生大鼠缺氧缺血性脑损伤后神经细胞凋亡持续至损伤后4周.     

新生大鼠缺氧缺血性脑损伤时细胞凋亡抑制蛋白1的变化

目的探讨在新生大鼠缺氧缺血性脑损伤(HIBD)细胞凋亡抑制蛋白1(cIAPl)的变化。方法建立新生大鼠HIBD动物模型，采用RT-PCR技术检测缺氧缺血(HI)后不同时间点缺血侧脑组织中cIAP1基因表达的变化。结果正常组中有cIAPl基因表达，HI组cIAPl基因表达明显下调，且随HI后时间的延长，cIAPl基因表达在HI后6h开始下调，24h下调最明显，48-72h有所回升。结论脑缺氧缺血引起的神经细胞凋亡可能与clAPl基因表达下调有关。     

新生大鼠缺氧缺血性脑损伤Caspase-1mRNA的表达变化

目的　研究新生大鼠缺氧缺血性脑损伤 (HIBD)后Caspase 1mRNA的表达变化。方法　制备新生大鼠左脑HIBD模型 ,用逆转录聚合酶链反应 (RT PCR)测定HIBD 12、2 4、72 ,96h不同时点脑皮质Caspase 1mRNA的表达 ,同时观察光镜下神经元坏死情况。结果　假手术对照组有少量Caspase 1mRNA表达 ,HIBD 12hCaspase 1mRNA的表达仍较少 ,与对照组相比无显著性差异 (P >0 0 5 ) ,HIBD 2 4～ 96hCaspase 1mRNA的表达逐渐增多 ,达高峰 ,同其他各组相比均有显著性差异 (P <0 0 5 )。光镜下HIBD 2 4～ 96h神经元坏死明显加重。结论　新生大鼠HIBD可诱导Caspase 1mRNA的表达 ,可能参与了新生儿HIBD的形成。     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

目的 探讨新生大鼠缺氧缺血性脑损伤(HIBD)的发生机制.方法 建立新生大鼠HIBD模型,随机分为假手术组及HIBD 6 h、12 h、24 h、48 h、72 h组,每组6只.观察脑组织大体病理学改变.采用Real-time Q-PCR方法测定大鼠脑组织MMP-9 mRNA和TIMP-1 mRNA表达.结果 (1)新生大鼠HIBD后12～48 h脑水肿明显,可见点状软化坏死灶.(2)假手术组大鼠MMP-9 mRNA表达水平极低,HIBD组大鼠在缺氧缺血6 h表达开始增高,24 h达高峰,此后渐渐下降,但72 h仍维持较高的水平,与假手术组相比差异有非常显著性(P＜0.01).(3)假手术组大鼠TIMP-1 mRNA表达水平极低,HIBD组大鼠在经历缺氧缺血6、12、24h,TIMP-1 mRNA表达水平有微弱升高,与假手术组相比差异有显著性(P＜0.05),但48 h后TIMP-1 mRNA表达下降到假手术组水平(P＞0.05).(4)MMP-9 mRNA/TIMP-1 mRNA比值在假手术组接近1:1,HIBD组缺氧缺血12 h后比值升高,在48 h达到高峰,72 h有所下降,但仍高于假手术组(P＜0.01).结论 新生大鼠HIBD后可诱导MMP-9 mRNA表达,而MMP-9 mRNA和TIMP-1 mRNA表达的失衡可能参与了HIBD的发病过程.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

高浓度氧对新生鼠肺血红素加氧酶-1蛋白表达的影响

目的　探讨高浓度氧对新生鼠肺损伤及肺血红素加氧酶 1(HO 1)蛋白表达的影响。方法　将生后 4～ 7d新生SD大鼠 5 7只随机分为 0、2 4、4 8、72h空气对照组和 2 4、4 8、72h高氧暴露组 ,分别置于空气中和常压高氧舱 (氧浓度 92 %～ 94 % )中 ,后断头处死后取肺组织 ,对肺组织切片在光镜、电镜下进行病理组织学观察 ,对肺组织湿 /干重比值进行比较 ,采用免疫组织化学分析对HO 1蛋白表达进行半定量及定位分析。结果　高氧组与空气对照组比较 ,肺组织有明显水肿、出血和炎症 ,电镜下观察病变主要在毛细血管内皮细胞 ;高氧 72h组肺组织湿 /干重比值 (7.97± 1.18)较 72h空气对照组 (6 .4 0± 0 .37)明显升高 (P <0 .0 5 ) ;高氧 72h组肺组织HO 1蛋白表达 (0 .5 0 4± 0 .0 6 2 )较 72h空气对照组 (0 .345± 0 .0 2 4 )明显升高 (P <0 .0 1) ;高氧暴露组HO 1蛋白呈强阳性表达 ,主要分布在支气管、肺泡上皮细胞和肺泡巨噬细胞。结论　高浓度氧可引起新生鼠肺损伤 ,且高浓度氧可引起新生鼠肺HO 1蛋白表达上调 ,证明HO 1参与新生鼠高氧肺损伤的病理生理过程     

新生大鼠缺氧缺血性脑损伤的亚低温治疗

目的　研究亚低温对缺氧缺血性脑损伤的保护作用 ,探讨亚低温治疗的最佳时机、深度、持续时间。方法　Wistar 7日龄新生大鼠 ,随机分为 :1) 2 9℃低温干预组、34℃低温干预组、常温 (37℃ )恢复组、正常对照组 (假手术组 ) ;2 ) 2 4h低温干预组、4 8h低温干预组、72h低温干预组、常温 (37℃ )恢复组、正常对照组 (假手术组 ) ;3)缺氧缺血后 0min起始低温干预组、6 0min起始低温干预组、12 0min起始低温干预组、6h起始低温干预组、常温 (37℃ )恢复组、正常对照组 (假手术组 )。每组均 2 0只大鼠均于缺氧缺血后 78h处死 ,测定脑组织含水量及微管相关蛋白 2 (MAP 2 )免疫组织化学染色 ,计算脑损伤程度。结果　 1) 2 9℃低温干预效果优于 34℃低温干预效果。 2 ) 72h低温干预效果优于 2 4、4 8h低温干预。 3)缺氧缺血后立即低温干预效果好 ,延迟 6h的低温干预仍有效。结论　缺氧缺血后立即 2 9℃低温干预 72h有显著脑保护作用     

缺氧缺血性脑损伤大鼠脑内bcl-2基因表达与细胞凋亡的关系

目的 观察bcl-2基因在缺氧缺血性脑损伤(HIBD)后细胞凋亡中的表达，探讨新生大鼠HmD后神经细胞凋亡的分子机制。方法 54只7日龄新生SD大鼠随机分为1个对照组和8个实验组。给动物吸入含有92％氮气和8％氧气混合气体建立新生大鼠HIBD动物模型，分另q在脑损伤后不同时间点(0．5、1、3、6、12、24、48、72h等)断头处死动物，取海马组织，用免疫组织化学方法检测海马脑神经细胞凋亡及bcl-2基因表达情况。结果 HIBD1h内未见凋亡细胞出现，3h开始出现，并在48h达高峰，之后逐渐下降。bcl-2蛋白阳性细胞在HIBD后立即出现，6h达到高峰，之后渐下降。结论 HIBD后bd-2基因表达在脑神经细胞凋亡过程中起一定作用。在一定时间范围内,bcl-2基因表达与脑神经细胞凋亡呈负相美。     

早期环境刺激对缺氧缺血性脑损伤大鼠学习记忆的影响

目的探讨生命早期丰富环境和触摸干预对缺氧缺血性脑损伤(HIBD)大鼠空间参考学习记忆能力及海马CA1区神经元数量的影响。方法生后7 d大鼠,建立HIBD动物模型,随机分为未干预组、丰富环境组、早期触摸组、联合干预组;另设假手术组,每组各14只大鼠。HIBD后7 d开始给予大鼠不同干预,于生后35 d行Morris水迷宫测试;同时,采用尼氏染色法观察各组大鼠海马CA1区神经元数量的变化。结果在Morris水迷宫隐蔽平台测试中,丰富环境组和联合干预组大鼠到达平台的平均潜伏期时间明显短于未干预组和早期触摸组,差异有统计学意义(P均<0.05);而早期触摸组与未干预组的差异无统计学意义。在Morris水迷宫探索测试中,丰富环境组和联合干预组大鼠在目标象限停留的百分比较未干预组显著增高,差异有统计学意义(P均<0.01),而早期触摸组和未干预组的差异无统计学意义。HIBD大鼠损伤侧海马CA1区神经元较假手术组明显减少,差异有统计学意义(P<0.001);其中联合干预组和丰富环境组大鼠损伤侧海马CA1区神经元的数目较未干预组和早期触摸组增加,差异有统计学意义(P<0.05);丰富环境组大鼠非损伤侧神经元数目增加,与其他各组比较差异有统计学意义(P<0.05)。结论新生仔鼠HIBD后1周开始的丰富环境仍可促进仔鼠脑功能恢复;新生仔鼠HIBD后早期短暂的触摸并不能增加丰富环境干预的疗效。     

缺氧缺血性脑病新生大鼠心肌血红蛋白加氧酶-1 mRNA表达与心肌细胞凋亡的关系

目的探讨HIE新生大鼠心肌血红蛋白加氧酶-1(HO-1)mRNA的表达及其与心肌细胞凋亡的关系。方法7日龄SD大鼠制备HIE经典模型。分为HIE组、HIE+Znpp组和对照组。采用原位杂交法观测其不同时间点各组HIE新生大鼠心肌细胞HO-1mRNA表达,采用图像分析半定量法检测其阳性强度,原位缺口末端标记(TUNEL)法检测其凋亡心肌细胞。结果1.HIE组心肌细胞HO-1mRNA表达6h开始上调(P<0.05),12h达高峰,48h开始略有下降,72h后仍高于对照组(Pa<0.01);与对照组比较,HIE+Znpp组心肌细胞HO-1mRNA表达下调,48h开始升高,72h后略低于对照组(P<0.05)。2.HIE组心肌细胞凋亡6h开始升高,48h达高峰,72h后略降低;HIE+Znpp组心肌细胞凋亡6h开始升高,12h达高峰,24h后略降低,但仍高于对照组和HIE组(P<0.01,0.05)。结论HIE新生大鼠心肌HO-1mRNA表达增加,可能降低了心肌细胞凋亡,提示HO-1参与HIE时机体对心肌细胞保护机制之一。     

血红素加氧酶-1抑制哮喘气道炎症的研究

目的探讨血红素加氧酶-1（heme oxygenase-1,HO-1）在小鼠支气管哮喘模型中的抗炎作用。方法用卵清蛋白（OVA）致敏、激发小鼠建立哮喘动物模型,并在致敏、激发过程中分别经Heroin、SnPP处理。分别测定激发后各组动物血清OVA特异性IgE（OVA-SIgE）、支气管肺泡灌洗液（bronchial alveolar lavage fluid,BALF）中细胞总数和嗜酸性粒细胞（eosinophil,EOS）,结合病理切片分析气道炎症状况。结果OVA组、Heine组、SnPP组血清OVA—SIgE和BALF中细胞总数及EOS数明显高于正常对照组,但Heine组IgE水平及BALF中细胞总数和EOS数明显低于OVA组;而OVA组和SnPP组间IgE水平及BALF中细胞总数和EOS数差异无显著性;病理切片显示OVA组、Heroin组、SnPP组气道组织均以嗜酸性粒细胞浸润为主,但Heroin组气道炎症仍明显轻于OVA组和SnPP组。结论用Heroin诱导HO-1高表达后血清OVA-SIgE明显下降,气道炎症减轻,提示HO-1在支气管哮喘中具有抗炎作用。     

缺氧缺血性脑损伤新生大鼠心肌细胞凋亡及凋亡蛋白Bax、Bcl-2表达的变化

目的 了解缺氧缺血性脑损伤新生大鼠心肌细胞凋亡及Bax、Bcl-2蛋白表达的变化.方法 通过结扎7 日龄新生大鼠一侧颈总动脉,吸入低浓度氧复制缺氧缺血性脑损伤(HIBD)的动物模型,并没假手术对照(NC)组,两组分别于HIBD后1 h、4 h、12 h、24 h、48 h、72 h、7 d取心脏组织,应用TUNEL法检测心肌细胞凋亡,SP法检测心肌细胞Bax、Bcl-2蛋白的表达.结果 NC组偶见心肌阳性凋亡细胞1～4个/mm~2,各时间点阳性细胞数差异无统计学意义(F=0.5,P>0.05).HIBD组12 h心肌阳性凋亡细胞开始增多,为(14.40±3.21)个/mm~2;72h达高峰,为(26.80 ±2.28)个/mm~2,12～72 h各时间点阳性凋亡细胞明显高于NC组(P<0.05);7 d阳性细胞数减少,但仍高于NC组.NC组大鼠心肌组织Bax呈阳性表达,Bcl-2呈弱阳性表达.HIBD组Bax于24 h开始增高.72 h表达最明显,7 d时表达有所降低,24 h～7 d表达高于NC组(P<0.05);Bel-2于24 h表达开始增高,以后缓慢增高,72 h达高峰,24 h～7 d较NC组表达增高,差异有统计学意义(P<0.05).HIBD组Bcl-2/Bax比值逐渐降低.Bax、Bcl-2的表达与凋亡细胞数之间均星直线正相关(r=0.921、0.980,P均<0.01).Bcl-2/Bax的比值与凋亡细胞数无相关性(r=0.702,P>0.05).结论 HIBD新生大鼠心肌细胞存在凋亡,心肌细胞Bax、Bcl-2蛋白表达增加,且与心肌细胞凋亡有关.     

药物干预幼大鼠缺氧缺血性脑损伤与p53蛋白表达的研究

目的通过检测缺氧缺血性脑损伤(HIBD)幼大鼠脑组织中p53蛋白的表达和一氧化氮(NO)、一氧化氮合酶(NOS)、超氧化物歧化酶(SOD)含量,探讨HIBD的发病机制;了解神经节苷酯(GM1)和胞二磷胆碱干预对HIBD的影响。方法80只Wistar幼大鼠随机分四组;对照组、缺氧缺血组、GM1组、胞二磷胆碱组。17日龄制作HIBD模型,24 h后处死检测脑组织中p53蛋白的表达和NO、NOS、SOD含量及组织形态学的变化。结果缺氧缺血组NO、NOS含量高于其他三组(P<0.05);缺氧缺血组与胞二磷胆碱组SOD含量低于对照组和GM1组(P<0.05);缺氧缺血组p53蛋白表达高于其他三组(P<0.01),GM1和胞二磷胆碱组p53蛋白表达高于对照组(P<0.01);组织形态学改变显示,缺氧缺血组变性、坏死严重,GM1组与胞二磷胆碱组次之,对照组正常。结论NO和自由基引起的组织损伤可能诱导p53蛋白表达导致HIBD。GM1和胞二磷胆碱能改善脑组织NO、NOS、SOD含量和p53的表达,提示GM1和胞二磷胆碱对HIBD有一定的保护作用。     

碱性成纤维细胞生长因子对新生大鼠缺氧缺血性脑损伤的作用

目的 探讨碱性成纤维细胞生长因子(bFGF)对新生儿缺氧缺血性脑损伤(HIBD)的防治作用。方法 7日龄SD大鼠30只，随机分为3组：1．伪手术组；2．HIBD组；3．bFGF治疗组。各组24h后断头取脑组织，进行病理学检查，并测定脑组织中水分、钙、谷氨酸(G1u)、天门冬氨酸(Asp)含量。结果 1．组2与组l相比，其脑组织水分、钙、G1u、Asp含量均增高(P＜0．01)，变性和坏死的细胞数明显增多；2．组3与组2相比，病理学改变明显减轻。结论 bFGF对新生大鼠HIBD具有明显的防治作用。     

碱性成纤维细胞生长因子对新生大鼠脑缺氧缺血后学习记忆能力的改善作用

目的评估碱性成纤维细胞生长因子(basicfibroblastgrowthfactor,bFGF)治疗新生大鼠缺氧缺血性脑损伤(hypoxic!ischemicbraindamage,HIBD)后学习记忆能力的改善作用。方法建立HIBD新生大鼠模型16只,随机分成治疗组、对照组,另取8只新生大鼠作假手术组。各组于生后30d开始进行Morris水迷宫测试,动态观察其学习记忆功能。结果对照组逃避潜伏期[(51.75±11.27)s]较治疗组[(40.32±11.48)s)]和假手术组[(36.58±10.83)s]明显延长(P<0.05);对照组拆除平台后跨越平台的次数[(2.34±2.42)次]较治疗组[(5.08±3.86)次]和假手术组[(7.03±3.62)次]明显减少(P<0.05)。结论bFGF可明显改善大鼠HIBD后的学习记忆能力。