辛醇预处理对红藻氨酸诱导的癫疒间大鼠海马神经元凋亡和胶质纤维酸性蛋白表达的影响

Influence of octanol protreatment on neuronal apoptosis and expression of glial fibrillary acidic protein in hippocampus in Kainic acid induced epileptic rats

目的观察缝隙连接阻断剂辛醇预处理对红藻氨酸(KA)诱导的癫疒间大鼠海马神经元凋亡和胶质纤维酸性蛋白(GFAP)表达的影响。方法 160只雄性SD大鼠随机分为KA组、辛醇组、生理盐水(NS)组和二甲基亚砜(DMSO)组,应用KA右侧杏仁核注射制作癫疒间大鼠模型;制模前30 min辛醇组腹腔注射辛醇溶液;制模后3 h、6 h、12 h、24 h和7 d应用原位末端标记(TUNEL)法和免疫组化染色法分别检测各组大鼠海马CA3区TUNEL和GFAP阳性细胞数。结果 KA组制模后6 h海马CA3区有TUNEL阳性细胞表达,并逐渐增多,7 d达高峰;辛醇组制模后在6 h～7 d TUNEL阳性细胞数明显少于KA组(均P<0.01);KA组海马CA3区GFAP阳性细胞数随时间而逐渐增多,各时间点明显多于辛醇组(均P<0.01)。结论辛醇神经保护作用的机制可能与抑制细胞缝隙连接间通讯,切断凋亡信号传播,以减少神经元凋亡有关。

Objective To observe the influence of gap junction blocking agent octanol protreatment on neuronal apoptosis and expression of glial fibrillary acidic protein （GFAP） in hippocampus in Kainic acid （ KA ） induced epileptic rats. Methods One hundred and sixty SD rats were randomly divided into KA group, octanol group, normal saline （NS） group and dimethylsuifoxide （DMSO） group. The epileptic model was established by KA injected in right amygdaloid nucleus of rats. Octanol was injected in rat＇s celiac in octanol group at 30 min before the model made. The apoptosis cells and GFAP expression in hippocampus CA3 region were detected by terminal deoxynuceotidy transferase mediated dUTP nick end labeling （TUNEL） and immunohistochemical staining method respectively at 3 h,6 h, 12 h, 24 h and 7 d after model made. Results In the hippocampus CA3 region, the TUNEL positive ceils were expressed at 6 h after the model made in KA group, gradually increased with the time, and reached peak at 7 d. Compared with KA group, the quantity of TUNEL positive cells in octanol group at 6 h - 7 d after models made were significantly less （ all P 〈 0. 01 ）. The quantity of GFAP positive cells in the hippocampus CA3 region in KA group were increased with time, and significantly more than octanol group at each time point（ all P 〈 0. 01 ）. Conclusion The neuroprotective mechanism of octanol may be related to inhibit the cell gap junction communication, cut off the apoptotic signals, and reduce neurons apoptosis.