中文摘要：

目的探讨丁苯酞(NBP)对慢性点燃癫痫大鼠模型海马神经元的保护作用。方法将40只雄性成年SD大鼠随机分为正常对照组、戊四氮组和NBP低中高组,每组8只。NBP低中高组在腹腔注射PTZ前30 min分别给予10、20、40 mg/kg,正常对照组和戊四氮组给予1 ml/kg植物油灌胃,后在每日的15∶00以35 mg/kg剂量腹腔注射戊四氮。约16 d建成慢性癫痫模型后处死,分别取出海马测定海马内硫化氢(H2S),并行免疫组化检测海马内5-羟色胺(5-HT)含量变化。结果与正常对照组比较,其他各组海马内5-HT均低于正常组,差异有极显著性(P<0.01)。与戊四氮组相比,NBP中剂量组和高剂量组能明显延长癫痫发作的潜伏期(均P<0.05),升高海马内5-HT(均P<0.01)。NBP高组与正常对照组相比,海马内H2S升高,差异有极显著性(P<0.01);NBP中剂量组与正常对照组比较,海马内H2S升高,差异无显著性(P>0.05);NBP中高剂量组与戊四氮组比较,海马内H2S明显升高,差异具有极显著性(P<0.01);戊四氮组和NBP低剂量组与正常对照组比较,海马内H2S降低,差异无显著性(P>0.05)。结论 NBP能减轻癫痫对海马神经元造成的损伤,其作用机制可能与丁苯酞升高海马内5-HT和H2S有关。

英文摘要：

Objective To explore the protective effect of butyphthalide on hippocampus neurons in epileptic rats .Methods 40 a-dult male SD rats were randomly divided into normal control , PTZ group, NBP low-dose, NBP medium-dose and NBP high-dose groups.The butyphthalide intervention groups was separately given 40, 20, 10 mg/kg butyphthalide 30 min before intraperitoneal injection of PTZ .The experiment was made at 15:00 every day.The hippocampus was taken out and observed by light microscopy and the levels of 5-hydroxytryPtamine ( HT) and hydrogen sulphide ( H2 S) were observed .Results The epileptic paroxysm latent period of NBP medium-dose and NBP high-dose groups were significantly prolonged (P<0.05,P<0.05).Compared with that of normal control group , the level of 5-HT in hippocampus of intervention group was decreased (P<0.01), the medium-dose and high-dose NBP significantly raised the level of 5-HT(all P<0.01,P<0.01) compared with PTZ.The high-dose NBP significantly raised the quantity of H2S(all P<0.01) in hippocampus compared with PTZ, the low-dose NBP and PTZ decreased the hippocampus H 2 S while the high-dose and medium-dose NBP raised the hippocampus H2S(P<0.01).Conclusions Butyphthalide could decrease hippocampus neuron damage caused by temporal epilepsy , which is related to the protective effect of butyphthalide of rising 5-HT and H2 S in hippocampus .