【摘要】 目的:探讨脑损伤后神经型一氧化氮合酶(nN 0S)对神经细胞凋亡的影响及其相关机制。方法:180只SD大鼠随机分成以下三组:假手术组、脑创伤组、7-硝基吲唑(7-N I)组,此三组分别划分为伤后3,6,12,24,48,72 h六个时相组,每个时相组均为10只大鼠,采用M arm arou法制造大鼠重型弥漫性颅脑创伤模型,运用原位末瑞标记TUNEL法和免疫组化法,观察三组不同时相点海马CA 1区的神经细胞凋亡情况和B cl-2的表达情况。结果:(1)假手术组偶见TUNEL阳性凋亡细胞及B cl-2阳性细胞。(2)脑创伤组,伤后各时相点均出现TUNEL阳性凋亡细胞及B cl-2阳性细胞,先上升后下降。(3)7-N I组,伤后6,12,24 h凋亡细胞明显下降而B cl-2阳性细胞却明显上升(同脑创伤组比较P<0.05)。结论:在脑损伤的早期,nNO S能够通过抑制B cl-2的表达来促进神经细胞的凋亡。更多还原

【Abstract】 Objective To investigate the effects of nNOS on the neuronal apoptosis after traumatic brain injury and the related mechanism.Methods One hundred and eighty male SD rats were randomly divided into 3 groups: fake operation group,trauma group,7-NI(the inhibitor of nNOS)group.The groups were divided into 6 subgroups according to the time phase after brain injury,which was 3 h,6 h,12 h,24 h,48 h and 72 h respectively.Each subgroup had 10 rats.Marmarou model of severe brain injury in rats were used to investigate the neuronal apoptosis,the expression of Bcl-2 in the hippocampal CA1 region of each time point after brain injury by TUNEL situ and immunohistochemistry.Results ① In fake operation,TUNEL positive cells and Bcl-2 positive cells could be observed occasionally.②In trauma group,TUNEL positive cells and Bcl-2 positive cells could be observed at each time point after injury.③In 7-NI group,the number of TUNEL positive cells at 6,12,and 24 h after injury was decreased significantly in comparison with that of trauma group(P<0.05),but Bcl-2 positive cells increased significantly.Conclusion nNOS can promote the neuronal apoptosis by inhibiting the expression of bcl-2 during the earlier period after brain injury.更多还原