SB203580对弥漫性脑创伤大鼠海马区Homer1a表达和神经细胞凋亡的影响及其作用机制  

Effects of SB203580 on Homer1a expression and nerve cell apoptosis in hippocampus of rats after diffuse brain injury and its mechanism

作　　者：赵雅宁[1] 李建民[2] 景丽伟[1] 张盼[1] 陈长香[1] 李淑杏[1] 刘文倩[2] 

机构地区：[1]河北联合大学护理与康复医学院,河北唐山063000 [2]河北联合大学附属医院神经外科,河北唐山063000

出　　处：《吉林大学学报（医学版）》2014年第2期243-247,I0001,共6页Journal of Jilin University：Medicine Edition

基　　金：河北省科技厅科研基金资助课题(20276102D);河北省教育厅科研基金资助课题(ZD2010106)

摘　　要：目的:探讨SB203580对弥漫性脑创伤(DBI)大鼠海马区Homer1a表达和神经细胞凋亡的影响,阐明DBI后p38MAPK和Homer1a作用机制及SB203580的脑保护作用。方法:96只雄性Sprague-Dawlley大鼠分为对照组(n=24,大鼠只进行乙醚麻醉而不致伤)、DBI组(n=40,Marmarou’s法建立大鼠DBI模型)和SB203580组(n=32,腹腔注射SB203580,0.01μg·kg-1)。采用电镜检测大鼠海马区神经细胞形态变化;采用免疫组织化学法检测大鼠海马CA1区磷酸化p38MAPK和Homer1a阳性细胞率;采用TUNEL法检测各组大鼠海马区神经细胞凋亡指数(AI)。结果:与对照组比较,DBI组大鼠各时间点(伤后6、24、48和72h)磷酸化p38MAPK和Homer1a阳性细胞率增高(P<0.05),神经细胞AI升高(P<0.05),其中磷酸化p38MAPK和Homer1a阳性细胞率24h达高峰,神经细胞AI 72h达高峰;与DBI组比较,SB203580组大鼠各时间点磷酸化p38MAPK阳性细胞率下降(P<0.05),Homer1a阳性细胞率显著增加(P<0.05),神经细胞AI降低(P<0.05)。结论:SB203580可降低DBI大鼠海马区神经细胞凋亡,其机制与抑制p38MAPK激活、提高Homer1a表达有关。Objective To explore the effects of SB203580 on the expression of Homerla and nerve cell apoptosis in hippocampus of rats after diffuse brain injury（DBI）, and to clarify the mechanism of p38MAPK and Homerla after DBI and the protective effect of SB203580. Methods 96 male Sprague-Dawlley rats were divided into control group （n= 24, only anesthesia without injury）, DBI group （n= 40, Marmarou＇ s method was used to establish DBI rat models）and SB203580 group（n=32, the rats were peritoneally injected with SB203580, 0.01 μg · kg^-1 ）. The morphological changes of nerve cells of the rats were observed under electron microscope; the positive cell rates of Homerla and phosphorylated p38MAPK in hippocampus CA1 of the rats were detected by immunohistochemistry and the apoptotic index（AI） of nerve cells of the rats was measured by TUNEL method. Results Compared with control group, the positive cell rates of phosphorylated p38MAPK and Homerla in DBI group were increased at each time point （6, 24, 48, and 72 h after DBI） （P〈0.05） and reached the peak at 24 h; the AI of nerve cells was increased obviously （P〈0.05） and reached the peak at 72 h. Compared with DBI group, the positive cell rate of phosphorylated p38MAPK was decreased while that of Homerla was increased and the AI o{ nerve cells was decreased obviously in SB203580 group（P〈0.05）. Oonclusion SB203580 can attenuate nerve cell apoptosis in hippocampus of the rats after DBI, and the mechanism is related to the inhibition of p38MAPK activation and increasing the expression of Homerla.

关 键 词：弥漫性脑创伤 有丝裂原活化蛋白激酶 Homer1a 细胞凋亡 

分 类 号：R651[医药卫生—外科学]