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目的探讨奥卡西平(OXC)对慢性癫癎幼鼠海马星形胶质细胞表达胶质纤维酸性蛋白(GFAP)的影响。方法 50只21日龄SD幼年雄性大鼠,随机分为5组:A组(阴性对照组)、B组(阳性对照组)、C组(OXC低剂量组)、D组(OXC中剂量组)、E组(OXC高剂量组),每组10只。A组每日腹腔注射等量9 g.L-1盐水;B组腹腔注射戊四氮(PTZ)40 mg.kg-1.d-1;C~E组腹腔注射PTZ 40 mg.kg-1.d-1后分别予OXC 100 mg.kg-1、OXC 200 mg.kg-1、OXC 300 mg.kg-1灌胃。连续用药21 d,观察幼鼠体质量、行为学表现;采用免疫组织化学方法检测幼鼠海马GFAP阳性星形胶质细胞的表达;应用实时荧光定量PCR方法检测幼鼠海马组织中GFAP mRNA表达。结果与A组相比,其他各组幼鼠均有癫癎发作,海马组织中均发现GFAP阳性细胞数量增多(P<0.01),GFAP mRNA的表达增加(P<0.01);与B组相比,C~E组幼鼠癫癎发作潜伏时间延长,发作级别低,点燃率低(Pa<0.05),GFAP阳性细胞数量逐渐减少(P<0.05),GFAP mRNA表达降低(P<0.05);与其他各组相比,E组幼鼠体质量增长缓慢(P<0.05)。结论 OXC对PTZ点燃的慢性癫癎引起的脑损伤有保护作用,其程度与剂量有关,但大剂量OXC会抑制幼鼠生长;OXC的这种神经保护作用可能是通过抑制星形胶质细胞表达GFAP实现的。
Objective To investigate the effect of oxcarbazepine (OXC) on glial fibrillary acidic protein (GFAP) expression in hippocampal astrocytes of chronic epileptic seizures. Methods Fifty male SD rats of 21 days old were randomly divided into 5 groups: A group (negative control group), B group (positive control group), C group (OXC low dose group), D group (OXC middle dose group ), Group E (OXC high dose group), 10 rats in each group. The rats in group A were injected intraperitoneally with the same dose of 9 gL-1 saline. Group B received intraperitoneal injection of pentazoton (PTZ) 40 mg.kg-1.d-1, while group C-E received intraperitoneal injection of PTZ 40 mg.kg-1.d -1 after OXC 100 mg.kg-1, OXC 200 mg.kg-1, OXC 300 mg.kg-1 orally. The rats were sacrificed for 21 days to observe the body weight and behavior of young rats. Immunohistochemistry was used to detect the expression of GFAP positive astrocytes in the hippocampus of young rats. GFAP mRNA expression in the hippocampus was detected by real-time fluorescence quantitative PCR. Results Compared with group A, all the other groups had epileptic seizures. The number of GFAP positive cells was increased in hippocampus (P <0.01) and the expression of GFAP mRNA was increased (P <0.01). Compared with group B (P <0.05), the number of GFAP positive cells decreased (P <0.05), and the expression of GFAP mRNA decreased (P <0.05). Compared with the control group, the latency of epileptic seizures increased, Compared with other groups, body weight of rats in group E increased slowly (P <0.05). Conclusion OXC can protect brain injury induced by PTZ-induced chronic epilepsy. The extent of OXC is dose-dependent, but high-dose OXC can inhibit the growth of juvenile rats. The neuroprotective effect of OXC may be through inhibition of astrocyte expression GFAP achieved.