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
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
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。
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.
