红藻氨酸致痫大鼠海马突触素的表达变化及辛醇的干预作用

Expressions of Synaptophysin in the Hippocampus of Rats Following Kainic Acid Induced Epileptic Seizure and Intervention Effect of Octanol

目的观察红藻氨酸(kainic acid,KA)致痫大鼠海马突触素(synaptophysin,SYP)表达的动态变化及辛醇的干预作用。方法将65只健康雄性SD大鼠随机分为空白对照组、模型组、辛醇干预组、二甲基亚砜(DMSO)组,空白对照组5只,余各组20只。采用KA注射于大鼠右侧杏仁核方法制备癫痫模型。造模前30 min给予大鼠腹腔注射辛醇进行干预,并观察辛醇干预前后大鼠行为学改变,采用免疫组化检测造模后不同时间点海马区SYP的表达水平。结果辛醇干预组大鼠出现湿狗样摇动(WDS)的潜伏期明显长于模型组(P<0.01),Patel评分显著低于模型组(P<0.01);模型组大鼠海马区SYP的表达于造模后1周逐渐升高,3周时达高峰,4周后开始下降;辛醇组大鼠海马区SYP的表达在各时间点均明显低于模型组(P<0.01)。结论辛醇可抑制KA致痫后大鼠海马区SYP表达的增高,具有明显的抗痫效应,提示辛醇抗痫机制可能与抑制SYP表达有关。

Objective To observe the kinetic changes of expression Synaptophysin （SYP） in the hippocampus and the impact of octanol in rats with epilepsy induced by kainic acid. Methods Five rats were chosen randomly as the control group, and the others were placed in the experimental group which was used for sham models of temporal epilepsy induced by kainic acid injected to the right amygdaloid nuclei. Rats in the experimental group were divided into three subgroups （n=20）： the model, octanol and dimethyl sulfoxide （DMSO） subgroup. The hippocampus of rats were sampled for analysis at the 1w, 2w, 3w, and 4w time-points after seizure activity. The changes of behaviour were recorded, and the expression of SYP in the hippocampus were observed by immunohistochemlstry and analyzed by computer image analysis technique. Results The wet dog shake eclipse period of the octanol group was obviously longer than the model group. There was statistically significant difference on comparison of Patel score between the octanol group and the model group （P〈0. 01）. The SYP expression in the hippocampus of the model group was increased gradually in 1-2w time-points, reached to the peak at 3w time-points, then decreased at 4w. The SYP expression of the octanol group, compared with the model group,at each point was lower （P〈0.01）. Conclusions SYP expression in the hippocampus of rats following kainic acid induced seizure activity were obviously increased. Octanol could decreased the expression of SYP, which could be part of mechanisms underlying the anti-epileptic effect.