摘要
目的研究海人酸(KA)对大鼠海马中生长相关蛋白-43(GAP-43)和神经细胞粘附分子(NCAM)表达的影响,以及托吡酯(TPM)对其的干预作用。方法将48只大鼠随机分成生理盐水(NS)组、4mg KA组、10mg KA组和10mg KA+TPM组(n=12),建立KA诱导颞叶癫大鼠模型和TPM干预模型,观察大鼠行为学改变,并通过RT-PCR和Western Blot的方法测定各组大鼠海马中GAP-43及NCAM的mRNA和蛋白表达水平。结果大鼠建模成功;4mg KA组、10mg KA组大鼠GAP-43及NCAM的mRNA和蛋白表达水平明显高于NS组(P<0.01),且10mg KA组高于4mg KA组(P<0.01);10mg KA+TPM组大鼠的GAP-43和NCAM表达明显低于10mg KA组(P<0.01)。结论KA能够诱导致大鼠海马GAP-43和NCAM表达上调,且与KA剂量有关,而TPM能够抑制KA诱导的GAP-43和NCAM的表达上调。
Objective To explore the effects of kainic acid （KA） on growth-associated protein 43 （GAP- 43） and nerve cell adhesion molecule （NCAM） expression in rats hippocampus, and the therapeutic roles of topiramate （TPM） to them. Methods 48 rats were randomly divided into NS, 4 mg KA, 10 mg KA and 10 mg KA＋ TPM groups （n = 12）, to found the models of rats temporal lobe epilepsy induced by KA and treated by TPM. The rats were observed in behavior. GAP43 and NCAM mRNA expression in the rats＇ hippoeampus were determined by RT-PCR, as well as protein expression by Western Blot. Results The rats models founded successfully, mRNA and protein expression of GAP-43 and NCAM were significantly higher in 4 mg KA and 10 mg KA groups than in NS group, when 10 mg KA group was more higher （P〈0. 01）. And corn pared to 10 mg KA group, GAP-43 and NCAM expression reduced in 10mg KA ＋ TPM group （P〈0.01）. Conclusions KA may up-regulate GAP-43 and NCAM expression in hippocampus of rats epilepsy induced by KA, and it＇s concerned with the dose of KA. Furthermore, TPM can inhibit this upregulating effect.
出处
《卒中与神经疾病》
2008年第6期350-353,共4页
Stroke and Nervous Diseases
基金
上海交通大学医学院科技基金项目(项目编号06×J21010)
