摘要
目的 观察亚低温对大鼠弥漫性脑损伤(DBI)后海马CA3区HSP70在蛋白质和mRNA水平的表达及细胞凋亡上的影响,探讨亚低温脑保护分子生物机制。方法 将大鼠随机分成空白对照、假手术、单纯DBI和DBI后亚低温治疗四组,按Marmarou氏方法制作大鼠DBI模型,采用免疫组化法、逆转录聚合酶链反应(RT-PCR)及流式细胞仪(FCM),分别观察各组动物脑海马CA3区HSP70在蛋白质和mRNA水平的表达及细胞凋亡率。结果 与对照组相比,大鼠DBI后海马CA3区HSP70表达水平及细胞凋亡率均升高(P<0.05);亚低温治疗后,大鼠脑海马CA3区HSP70表达水平较单纯DBI组显著增高(P<0.01),而细胞凋亡率则明显降低(P<0.05)。结论 亚低温对创伤性脑损伤的脑保护机制可能与促进HSP70表达,并减少神经细胞凋亡有关。
Objective To observe the effects of mild hypothermia on the expression of HSP70 protein and HSP70 mRNA and the cell apoptosis at CA3 area ofhippocampus in rats following experimental diffuse brain injury (DBI) and to explore the neuroprotective mechanism of mild hypothermia at molecular level. Methods The rats were divided into four groups: control, pseudo-operation, only DBI and post-DBl mild hypothermia treatment. Marmarou' s method was used to establish the animal model of DBI. Immunohistochemistry, RT-PCR and flow cytometer were separatively performed to examine the expression of HSP70 at protein and mRNA level and the cell apoptotic rate at CA3 area of hippocampus in each group. Results Compared to the control group, both the HSPT0 expression at protein and mRNA level and cell apoptotic ratio at CA3 area of hippocampus in rat brain increased following DBI (P<0.05). When the rats subjected to DBI were treated with the mild hypothermia, the HSP70 expression at protein and mRNA level significantly increased (P<0.01) in hippocampus CA3 area of rat brain, while the cell apoptosis rate decreased (P<0.05). Conclusion The neuroprotective effects of mild hypothermia on the traumatic brain injury may be correlated with the improvement of liSP70 protein and HSP70 mRNA expression as well as the decrease of the cell apoptosis in the injuryed brain tissue.
出处
《中华神经医学杂志》
CAS
CSCD
2004年第5期337-338,341,共3页
Chinese Journal of Neuromedicine
