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目的探讨钙释放激活钙离子通道(calcium release-activated calcium,CRAC)关键蛋白STIM1在幼年和成年大鼠外伤性癫痫中的表达差异及意义。方法取SD雄性幼年、成年大鼠各94只,按照完全随机设计分为成年、幼年假手术组:皮层注射生理盐水,各42只;成年、幼年模型组:铁离子皮层注射外伤性癫痫模型,各52只。建模后观察大鼠癫痫行为学表现;分别于6、24、72 h,7、14、21、28 d 7个时相点完全随机选取6只大鼠,处死取伤灶周边皮层脑组织,用实时荧光定量PCR、Western blot和免疫组织化学法分别检测STIM1的mRNA与蛋白的表达。结果模型组成年、幼年大鼠均出现典型痫性发作,幼鼠模型组建模成功率为91.3%,成鼠模型组建模成功率为84%(定义Racine评分3分及以上为建模成功)。幼鼠模型组比成鼠模型组发作次数明显增多(P<0.05),每次发作持续时间显著延长(P<0.05),发作程度较重。建模后各组STIM1的mRNA和蛋白表达都有明显增高,72 h达高峰(P<0.05),但幼鼠与成鼠相比较,STIM1的mRNA和蛋白在各时间点表达增高的趋势更加显著(P<0.05)。结论幼鼠较成鼠更容易发生外伤性癫痫,STIM1在幼鼠中较成鼠的表达也更高,提示STIM1表达增加、CRAC激活可能是幼鼠更易发生外伤性癫痫的机制之一。
Objective To investigate the difference and significance of STIM1, a key protein of calcium release-activated calcium (CRAC), in traumatic epilepsy in juvenile and adult rats. Methods 94 male and female SD rats were randomly divided into adult and juvenile sham operation groups. Cortical injection of normal saline (n = 42) was performed in each group. Adult and juvenile model groups were given iron ion cortex injection traumatic epilepsy model, 52 each. After modeling, we observed the behavior of epilepsy in rats. Six rats were randomly selected at 6, 24, 72 h, 7, 14, 21, 28 d respectively. The cerebral cortex tissues were harvested, Real-time quantitative PCR, Western blot and immunohistochemistry were used to detect the mRNA and protein expression of STIM1. Results The models were composed of typical epileptic seizures in juvenile rats. The successful rate of model establishment was 91.3% in young rats and 84% in model rats (defined as Racine score 3 and above) ). Compared with the model group, the number of seizures increased significantly (P <0.05), the duration of each seizure significantly prolonged (P <0.05), and the degree of seizure was heavier. After modeling, the mRNA and protein expressions of STIM1 in each group were significantly increased, reaching the peak at 72 h (P <0.05), but the mRNA and protein expressions of STIM1 increased more significantly at each time point (P <0.05). Conclusion Compared with adult rats, rats are more likely to develop traumatic epilepsy. STIM1 is also more expressed in young rats than normal rats, which suggests that STIM1 expression is increased. Activation of CRAC may be one of the mechanisms of traumatic epilepsy.