Carnosine is a dipeptide that scavenges free radicals, inhibits infammation in the central nervous system, and protects against ischemic and hypoxic brain damage through its anti-oxidative and anti-apoptotic actions. ...Carnosine is a dipeptide that scavenges free radicals, inhibits infammation in the central nervous system, and protects against ischemic and hypoxic brain damage through its anti-oxidative and anti-apoptotic actions. Therefore, we hypothesized that carnosine would also protect against white matter damage caused by subcortical ischemic injury. White matter damage was induced by right unilateral common carotid artery occlusion in mice. The animals were treated with 200, 500 or 750 mg/kg carnosine by intraperitoneal injection 30 minutes before injury and every other day after injury. Then, 37 days later, Klfiver-Barrera staining, toluidine blue staining and immunofluorescence stain- ing were performed. Carnosine （200, 500 mg/kg） substantially reduced damage to the white matter in the corpus callosum, internal capsule and optic tract, and it rescued expression of myelin basic protein, and alleviated the loss of oligodendrocytes. However, carnosine at the higher dose of 750 mg/kg did not have the same effects as the 200 and 500 mg/kg doses. These findings show that carnosine, at a particular dose range, protects against white matter damage caused by chronic cerebral ischemia in mice, likely by reducing oligodendroglial cell loss.展开更多
The Chinese compound Kaixin fieyu Fang can be used to treat vascular depression; however, the underlying mechanism remains unclear. This study established a rat model of chronic cerebral ischemia-caused white matter d...The Chinese compound Kaixin fieyu Fang can be used to treat vascular depression; however, the underlying mechanism remains unclear. This study established a rat model of chronic cerebral ischemia-caused white matter damage by ligation of the bilateral common carotid arteries. Rats received daily intragastric administration of a suspension of Kaixin ]ieyu Fang powder. After 3, 7 and 21 days of treatment, the degree of white matter damage in the cerebral ischemia rat model was alleviated, Bcl-2 protein and mRNA expression in brain tissue increased, and Bax protein and mRNA expression decreased. These results indicate that Kaixin Jieyu Fang can alleviate cere- bral white matter damage, and the underlying mechanism is associated with regulation of Bcl-2/ Bax protein and mRNA expression, which is one of possible mechanism behind the protective effect of Kaixin Jieyu Fang against vascular depression.展开更多
BACKGROUND： To date, animal models of white matter damage remain controversial. Mild grey matter damage should be the basis for animal models to investigate white matter disease. OBJECTIVE： To establish white matter...BACKGROUND： To date, animal models of white matter damage remain controversial. Mild grey matter damage should be the basis for animal models to investigate white matter disease. OBJECTIVE： To establish white matter damage in neonatal rats and evaluate feasibility of the established model by observing myelination and synaptic ultrastructure. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratory of Histology and Embryology of Guangzhou Medical College from December 2008 to May 2009. MATERIALS： H600 transmission electron microscopy was provided by Hitachi, Japan. METHODS： A total of 39 neonatal, Sprague Dawley rats were randomly assigned to normal control （n = 12）, sham-surgery （n = 12）, and white matter damage （n = 15） groups. White matter damage rats were subjected to right common carotid artery ligation, followed by inhalation of nitrogen oxygen gas mixture （6% oxygen） for 4 hours. MAIN OUTCOME MEASURES： Myelin sheath and synaptic ultrastructure in the injured （right） hippocampal CA1 region in 1-month-old rats were observed through the use of transmission electron microscopy, and pathological changes in the cerebral cortex and corpus callosum of the right hemisphere were detected by hematoxylin-eosin staining. RESULTS： Obvious tissue loss was observed in the corpus callosum of the injured （right） hemisphere. Injured oligodendrocytes and disrupted myelination were observed in the white matter damage group. However, synaptic length in the active zones, width of synaptic cleft, thickness of postsynaptic density, and curvature of the synaptic interface remained unchanged following injury, compared with the control and sham-surgery groups （P 〉 0.05）. CONCLUSION： The established white matter damage model resulted in changes in myelination and slightly altered synaptic ultrastructures. The model could function as an ideal model for white matter damage in neonatal rats.展开更多
非痴呆型血管性认知障碍(vascular cognitive impairment no dementia,VCIND)是认知障碍的早期阶段,认知损害尚未达到痴呆的标准。本文从中医“虚、痰、瘀”的病因病机进行阐述,脾肾亏虚为发病基础,痰瘀互结为致病因素,导致髓海不足,清...非痴呆型血管性认知障碍(vascular cognitive impairment no dementia,VCIND)是认知障碍的早期阶段,认知损害尚未达到痴呆的标准。本文从中医“虚、痰、瘀”的病因病机进行阐述,脾肾亏虚为发病基础,痰瘀互结为致病因素,导致髓海不足,清窍失养,发为痴呆。胆碱能通路与认知障碍的发生发展密切相关,包括神经递质乙酰胆碱的缺乏、脑白质病变影响胆碱能通路的网络连接以及胆碱能抗炎通路等。探讨中医虚痰瘀的病机演变与胆碱能通路发病机制之间的关系,有助于进一步发掘中医中药治疗在胆碱能通路的作用。展开更多
目的探讨早产儿脑白质损伤(WMD)发生率及临床表现;研究WMD早期S100B蛋白、神经元特异性烯醇化酶(NSE)及肌酸激酶脑型同工酶(CK-BB)的动态变化。方法选择2011年1月至10月临床资料完整的早产儿病例,生后24、72、120 h采静脉血,应用化学发...目的探讨早产儿脑白质损伤(WMD)发生率及临床表现;研究WMD早期S100B蛋白、神经元特异性烯醇化酶(NSE)及肌酸激酶脑型同工酶(CK-BB)的动态变化。方法选择2011年1月至10月临床资料完整的早产儿病例,生后24、72、120 h采静脉血,应用化学发光法检测S100B蛋白与NSE,酶联免疫吸附法检测CK-BB。据颅脑超声检查分为WMD组(18例)及无WMD作为对照组(53例)。结果早产儿中WMD发生率为25.35%。WMD组惊厥、呼吸暂停、肌张力改变所占比例均高于无WMD组(P均<0.05)。WMD组生后24、72、120 h S100B蛋白含量均高于无WMD组(P均<0.05);WMD组生后24 h NSE含量高于无WMD组(P<0.01),72、120 h两组差异无统计学意义(P均>0.05);WMD组生后24、72、120 h CK-BB含量均高于无WMD组(P均<0.05)。结论 WMD早产儿S100B蛋白、NSE及CK-BB在生后24 h内均升高,S100B蛋白与CK-BB升高持续时间长。展开更多
基金funded by the National Natural Science Foundation of China,No.81402904the Foundation of Shanghai Jiao Tong University School of Medicine,No.13XJ22001+1 种基金the Foundation of Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,No.13YJ11a grant from the Science and Technology Commission of Shanghai Municipality of China,No.13ZR1426900,15411963900
文摘Carnosine is a dipeptide that scavenges free radicals, inhibits infammation in the central nervous system, and protects against ischemic and hypoxic brain damage through its anti-oxidative and anti-apoptotic actions. Therefore, we hypothesized that carnosine would also protect against white matter damage caused by subcortical ischemic injury. White matter damage was induced by right unilateral common carotid artery occlusion in mice. The animals were treated with 200, 500 or 750 mg/kg carnosine by intraperitoneal injection 30 minutes before injury and every other day after injury. Then, 37 days later, Klfiver-Barrera staining, toluidine blue staining and immunofluorescence stain- ing were performed. Carnosine （200, 500 mg/kg） substantially reduced damage to the white matter in the corpus callosum, internal capsule and optic tract, and it rescued expression of myelin basic protein, and alleviated the loss of oligodendrocytes. However, carnosine at the higher dose of 750 mg/kg did not have the same effects as the 200 and 500 mg/kg doses. These findings show that carnosine, at a particular dose range, protects against white matter damage caused by chronic cerebral ischemia in mice, likely by reducing oligodendroglial cell loss.
基金supported by the National Natural Science Foundation of China,No.30672696,81072801the Natural Science Foundation of Beijing in China,No.7093129
文摘The Chinese compound Kaixin fieyu Fang can be used to treat vascular depression; however, the underlying mechanism remains unclear. This study established a rat model of chronic cerebral ischemia-caused white matter damage by ligation of the bilateral common carotid arteries. Rats received daily intragastric administration of a suspension of Kaixin ]ieyu Fang powder. After 3, 7 and 21 days of treatment, the degree of white matter damage in the cerebral ischemia rat model was alleviated, Bcl-2 protein and mRNA expression in brain tissue increased, and Bax protein and mRNA expression decreased. These results indicate that Kaixin Jieyu Fang can alleviate cere- bral white matter damage, and the underlying mechanism is associated with regulation of Bcl-2/ Bax protein and mRNA expression, which is one of possible mechanism behind the protective effect of Kaixin Jieyu Fang against vascular depression.
基金the Science and Technology Program of Medical Health of Guang-zhou, No. 2008-YB-173a Grant from Guangdong Provincial Health Depart-ment, No. A2009271
文摘BACKGROUND： To date, animal models of white matter damage remain controversial. Mild grey matter damage should be the basis for animal models to investigate white matter disease. OBJECTIVE： To establish white matter damage in neonatal rats and evaluate feasibility of the established model by observing myelination and synaptic ultrastructure. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Laboratory of Histology and Embryology of Guangzhou Medical College from December 2008 to May 2009. MATERIALS： H600 transmission electron microscopy was provided by Hitachi, Japan. METHODS： A total of 39 neonatal, Sprague Dawley rats were randomly assigned to normal control （n = 12）, sham-surgery （n = 12）, and white matter damage （n = 15） groups. White matter damage rats were subjected to right common carotid artery ligation, followed by inhalation of nitrogen oxygen gas mixture （6% oxygen） for 4 hours. MAIN OUTCOME MEASURES： Myelin sheath and synaptic ultrastructure in the injured （right） hippocampal CA1 region in 1-month-old rats were observed through the use of transmission electron microscopy, and pathological changes in the cerebral cortex and corpus callosum of the right hemisphere were detected by hematoxylin-eosin staining. RESULTS： Obvious tissue loss was observed in the corpus callosum of the injured （right） hemisphere. Injured oligodendrocytes and disrupted myelination were observed in the white matter damage group. However, synaptic length in the active zones, width of synaptic cleft, thickness of postsynaptic density, and curvature of the synaptic interface remained unchanged following injury, compared with the control and sham-surgery groups （P 〉 0.05）. CONCLUSION： The established white matter damage model resulted in changes in myelination and slightly altered synaptic ultrastructures. The model could function as an ideal model for white matter damage in neonatal rats.
文摘非痴呆型血管性认知障碍(vascular cognitive impairment no dementia,VCIND)是认知障碍的早期阶段,认知损害尚未达到痴呆的标准。本文从中医“虚、痰、瘀”的病因病机进行阐述,脾肾亏虚为发病基础,痰瘀互结为致病因素,导致髓海不足,清窍失养,发为痴呆。胆碱能通路与认知障碍的发生发展密切相关,包括神经递质乙酰胆碱的缺乏、脑白质病变影响胆碱能通路的网络连接以及胆碱能抗炎通路等。探讨中医虚痰瘀的病机演变与胆碱能通路发病机制之间的关系,有助于进一步发掘中医中药治疗在胆碱能通路的作用。
文摘目的探讨早产儿脑白质损伤(WMD)发生率及临床表现;研究WMD早期S100B蛋白、神经元特异性烯醇化酶(NSE)及肌酸激酶脑型同工酶(CK-BB)的动态变化。方法选择2011年1月至10月临床资料完整的早产儿病例,生后24、72、120 h采静脉血,应用化学发光法检测S100B蛋白与NSE,酶联免疫吸附法检测CK-BB。据颅脑超声检查分为WMD组(18例)及无WMD作为对照组(53例)。结果早产儿中WMD发生率为25.35%。WMD组惊厥、呼吸暂停、肌张力改变所占比例均高于无WMD组(P均<0.05)。WMD组生后24、72、120 h S100B蛋白含量均高于无WMD组(P均<0.05);WMD组生后24 h NSE含量高于无WMD组(P<0.01),72、120 h两组差异无统计学意义(P均>0.05);WMD组生后24、72、120 h CK-BB含量均高于无WMD组(P均<0.05)。结论 WMD早产儿S100B蛋白、NSE及CK-BB在生后24 h内均升高,S100B蛋白与CK-BB升高持续时间长。
