论文部分内容阅读
目的探讨奥卡西平对戊四氮致大鼠海马神经元凋亡的影响。方法 4周龄大鼠84只,随机分为4组:A组予9 g.L-1盐水(18只),B组予奥卡西平(18只),C组致后予9 g.L-1盐水(24只),D组致后予奥卡西平(24只)。C组、D组连续5 d腹腔注射戊四氮60 mg.kg-1.d-1,根据Racine分级观察大鼠发作情况,连续5 d出现Ⅳ～Ⅴ级癫发作,每次持续3～5 min为模型制备成功。第6天起,A组、C组腹腔注射9 g.L-1盐水,B组、D组予奥卡西平80 mg.kg-1.d-1灌胃。于喂药满9 d、15 d、21 d,处死动物取脑,做石蜡块,行HE、免疫组织化学染色。观察各组大鼠脑海马区神经细胞凋亡情况。结果 1.HE染色:光镜下,A组、B组脑组织形态学未见明显差别。C组可见细胞空泡样变性,胞膜内陷。D组可见大量凋亡细胞,细胞层数增多。2.Bcl-2表达:A组、B组大鼠海马区均有Bcl-2少量表达,在9 d、15 d、21 d时间点,组间比较差异均无统计学意义;C组Bcl-2阳性细胞数在9 d、15 d、21 d较A组、B组增多;D组Bcl-2的表达在9 d、15 d、21 d时较其他3组均显著增多;C组、D组Bcl-2因子早期显著表达后,迅速下降,但在21 d时仍显著高于A组、B组。3.Bax表达:A组、B组、D组3组大鼠海马区均有Bax表达,组间比较、组内各个时间点比较差异均无统计学意义。C组Bax阳性细胞数表达在9 d、15 d较其他3组均增多,差异有统计学意义,而在21 d时与上述3组比较无统计学差异。结论奥卡西平能减轻癫所致的海马部位神经元损伤,促进凋亡因子Bcl-2表达,抑制Bax表达。对大鼠海马区神经元具有保护作用。
Objective To investigate the effects of oxcarbazepine on the apoptosis of hippocampal neurons induced by pentylenetetrazole in rats. Methods Eighty-four 4-week-old rats were randomly divided into 4 groups: group A received 9 gL-1 saline (18), group B received oxcarbazepine (18) (24), and group D was given oxcarbazepine 24 (24). Rats in group C and group D were injected intraperitoneally with pentylenetetrazol 60 mg.kg-1.d-1 for 5 consecutive days. According to Racine’s grading, the occurrence of grade IV-V epilepsy was observed for 5 consecutive days, 5 min for the successful preparation of the model. On day 6, group A and group C received intraperitoneal injection of 9 g · L-1 saline, and group B and group D received oxcarbazepine 80 mg.kg-1.d-1 orally. At 9 d, 15 d and 21 d after feeding, the animals were sacrificed and their brains were removed. Paraffin blocks were obtained and subjected to HE and immunohistochemical staining. The apoptosis of neurons in hippocampus of rats in each group was observed. Results 1. HE staining: Under light microscope, there was no significant difference in brain histomorphology between group A and group B. C group showed vacuolar degeneration, membrane invagination. D group showed a large number of apoptotic cells, cell layers increased. Bcl-2 expression: A group, B group rats Bcl-2 expression in small amounts, at 9 d, 15 d, 21 d time point, there was no significant difference between the two groups; C group Bcl- 2 positive cells increased at 9 d, 15 d and 21 d compared with those in group A and group B. The expression of Bcl-2 in group D increased significantly at 9 d, 15 d and 21 d compared with the other three groups. In group C, D The expression of Bcl-2 decreased rapidly at early stage, but was still significantly higher than that of group A and B at 21 d. Bax expression: Bax expression was detected in hippocampus of group A, group B and group D, and there was no significant difference between groups at all time points. The expression of Bax positive cells in group C increased on the 9th and 15th days compared with the other three groups, and the difference was statistically significant, but there was no significant difference between the three groups at 21 days. Conclusion Oxcarbazepine can reduce the damage of neurons in hippocampus induced by epilepsy, promote the expression of Bcl-2 and inhibit the expression of Bax. Protect neurons in hippocampus of rats.