目的:探讨皮质发育障碍(Disorder of cortical developments,DCDs)模型鼠海马神经元的凋亡机制。方法:利用卡莫司汀(BCNU)诱导建立SD大鼠皮质发育障碍动物模型,在出生后0d(P0)、15d(P15)、30d(P30)、45d(P45)和60d(P60)时,采用TUNEL检...
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目的:探讨皮质发育障碍(Disorder of cortical developments,DCDs)模型鼠海马神经元的凋亡机制。方法:利用卡莫司汀(BCNU)诱导建立SD大鼠皮质发育障碍动物模型,在出生后0d(P0)、15d(P15)、30d(P30)、45d(P45)和60d(P60)时,采用TUNEL检测海马区神经元凋亡,RT-PCR方法和免疫组化分别对8只模型鼠和正常鼠检测海马区Bcl-2和Bax的在mRNA和蛋白水平的表达,并结合图像分析系统进行结果分析。结果:成功建立SD大鼠皮质发育障碍动物模型;与对照组比较,TUNEL、免疫组化和RT-PCR检测结果显示:P0模型鼠组海马区神经元凋亡无明显变化,P15、P30、P45、P60模型组神经元凋亡逐渐加重,有显著差异(P<0.05),且随存活时间延长,模型组海马神经元Bax表达逐渐增强,Bax/Bcl-2比值较对照组增高,具有显著统计学意义(P<0.05)。结论:皮质发育障碍模型鼠海马区存在显著的神经元凋亡,Bcl-2和Bax参与了其凋亡过程;皮质发育障碍模型鼠海马神经元凋亡可能参与了皮质发育障碍所致的癫痫及难治性癫痫的发病机制。
Objective To study the neuroprotective mechanism of minocycline against vascular cognitive impairment after cerebral ischemia. Methods The rat model with vascular cognitive impairment was established by permanent bila...
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Objective To study the neuroprotective mechanism of minocycline against vascular cognitive impairment after cerebral ischemia. Methods The rat model with vascular cognitive impairment was established by permanent bilateral common carotid artery occlusion （BCCAO）. The observing time-points were determined at 4, 8 and 16 weeks after BCCAO. Animals were randomly divided into sham-operated group （n = 6）, model group （subdivided into 3 groups： 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6）, and minocycline group （subdivided into 3 groups： 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6）. Minocycline was administered by douche via stomach after BCCAO until sacrifice. Glial fibrillary acidic protein （GFAP） was examined by Western blotting and immunohistochemistry. Levels of cyclooxygenase-2 （COX-2） and nuclear factor-kappaB （NF-κB） were measured by immunohistochemistry. IL-1β and TNF-α levels were tested with ELISA method. Results Levels of GFAP, COX- 2, NF-κB, IL-1β and TNF-α were all up-regulated after permanent BCCAO, which could be significantly inhibited by minocycline. Conclusion Minocycline could ameliorate the inflammation and oxidative stress in the hippocampus of the vascular cognitive impairment rat model.
为了解释多发性硬化(multiple sclerosis,MS)的临床和病理之间的矛盾,引入了功能MRI检查,其中磁共振波谱(proton magnetic resonance spectroscopy,1^H-MRS)检查为其中最重要的技术之一。1^H-MRS对MS脑内病灶提供了一种无创性测量方法,...
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为了解释多发性硬化(multiple sclerosis,MS)的临床和病理之间的矛盾,引入了功能MRI检查,其中磁共振波谱(proton magnetic resonance spectroscopy,1^H-MRS)检查为其中最重要的技术之一。1^H-MRS对MS脑内病灶提供了一种无创性测量方法,波谱数据分别代表了MS特有的相关事件如脱髓鞘、炎性反应、轴索或神经元的破坏。1^H-MRS研究将MS病变从白质延伸到了灰质,[第一段]
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