N-myc在大鼠急性痫性发作模型中的表达及其意义

N-myc expression and its significance in rat model of acute seizures

目的 探讨在氯化锂-匹罗卡品诱导大鼠急性痫性发作模型中N-myc表达及其意义。方法 健康Wistar雄性大鼠45只,随机分为生理盐水对照组、地西泮干预组和致痫1 h～9 d组(根据致痫后的不同时点分7个组),共9组,每组5只。采用氯化锂-匹罗卡品联合腹腔注射急性致痫大鼠模型,常规HE染色观察实验大鼠脑组织的形态学改变,免疫组化染色法观察脑内N-myc表达产物分布及其含量变化。结果 致痫1d～9d组尤其致痫6d和9d两组可见到脑组织损伤性改变,海马区重于皮质区。生理盐水对照组N-myc几乎无表达,地西泮干预组低表达,致痫组表达增多,尤其以致痫1d组和致痫3d组最为明显。结论 急性痫性发作或癫痫持续状态可导致脑组织损伤性改变,以海马结构等易损区为明显。N-myc表达及其表达量可能与急性痫性发作后脑损伤及其受累部位有关。

Objective To explore the N-myc expression and its significance in rat model of acute seizures induced by lithium-pilocarpine. Methods Healthy 45 Wistar male rats were divided into 0.9% sodium chloride control group, diazepam interferential group and seven seizure-induced groups randomly (5 rats in each group). Histomorphometric changes and distribution and quantity of N-myc proteins were inspected in the experimental rats. Resuits In the seizure-induced 1 d～9 d groups, especially in 6 d and 9 d groups, had severe brain damage, which was worse in the hippocampus than in cortex. There was no expression of N-mye in 0.9% sodium chloride control group; In the diazepam interferential group, expression of N-myc was lower, While in the seizure-induced groups, especially in 1 d and 3 d groups, there was overexpression. Conclusions Acute seizures or status epilepticus could lead to brain damage, especially in the hippocampal vulnerable areas; N-myc expression and its quantity might be associated with brain damage and its distribution after acute seizures.