厄多司坦对癫痫大鼠海马氧化应激及BDNF表达的影响
发布时间：2019-02-13 09:53
【摘要】：目的： 通过观察厄多司坦对癫痫模型大鼠海马中超氧化物岐化酶(SOD)活力、丙二醛(MDA)含量的变化和神经元的病理损害程度及脑源性神经营养因子水平变化,探讨其抗癫痫病作用的可能机理。 方法: 选取健康雄性SD大鼠40只,分为正常对照组、戊四氮组、厄多司坦干预组和丙戊酸钠组,每组各10只。腹腔注戊射四氮诱导癫痫发作,厄多司坦干预组和丙戊酸钠组在点烯癫痫之前,各使用厄多司坦(50mg/Kg)和丙戊酸钠(100mg/Kg)灌胃进行预处理。右侧海马测定SOD活力及MDA含量,左侧海马经免疫组化染色方法观察BDNF阳性细胞分布情况,HE染色观察大鼠海马神经元损伤情况。 结果： 1.大鼠海马SOD活力及MDA水平：癫痫发作后戊四氮组与对照组比较,SOD活力显著降低(p0.01),厄多司坦干预组较戊四氮组升高(p0.01),厄多司坦干预组与丙戊酸钠组比较,无明显差异(p0.05)；致四氮组与对照组比较MDA含量显著长高(p0.01),厄多司坦干预组较戊四氮组降低(p0.01),厄多司坦干预组与丙戊酸钠组比较无明显差异(p0.05)。 2.HE染色结果：对照组大鼠海马神经元排列紧密,边缘清晰,胞浆透明,细胞核形态正常,无坏死性神经元。戊四氮组大鼠海马神经元排列散乱,数目减少,胞体皱缩及核固缩,出现大量坏死性神经元,厄多司坦干预组和丙戊酸钠组可见散在坏死性神经元。戊四氮组与对照组比较,有显著差异(p0.01)；厄多司坦干预组与戊四氮组比较,有差异(p0.05)；厄多司坦干预组与丙戊酸钠组比较,无明显差异(p0.05)。 3.BDNF阳性表达：戊四氮组与对照组比较,染色强度显著增强(p0.01),与厄多司坦干预组比较,染色强度较降低(p0.05)；厄多司坦干预组与丙戊酸钠组比较,无明显差异(p0.05)。 结论: 厄多司坦能减轻癫痫大鼠海马氧化应激水平,预处理不能完全防止癫痫发生,但可以减轻神经元损伤程度,提示其神经保护作用的存在。厄多司坦可能通过清除戊四氮点燃大鼠海马中多余的自由基及增加海马BDNF的表达而而参与神经元保护机制。
[Abstract]:Objective: to observe the changes of superoxide dismutase (SOD) activity, malondialdehyde (MDA) (MDA) content in hippocampus of epileptic model rats, the degree of neuronal pathological damage and the level of brain-derived neurotrophic factor (BDNF). To explore the possible mechanism of its antiepileptic effect. Methods: forty healthy male SD rats were divided into normal control group, pentylenetetrazol group, erdostam intervention group and sodium valproate group with 10 rats in each group. The epileptic seizures were induced by intraperitoneal injection of pentylenetetrazole, and pretreated by oral administration of 50mg/Kg and 100mg/Kg, respectively, in the Edostam intervention group and sodium valproate group. The activity of SOD and the content of MDA were measured in the right hippocampus, the distribution of BDNF positive cells in the left hippocampus was observed by immunohistochemistry, and the damage of hippocampal neurons was observed by HE staining. Results: 1. SOD activity and MDA level in hippocampus of rats: compared with control group, SOD activity in pentylenetetrazol group was significantly lower than that in control group (p0.01), and that in erdostam intervention group was higher than that in pentylenetetrazol group (p0.01), and that in erdostam intervention group was higher than that in pentylenetetrazol group (p0.01). There was no significant difference (p0.05). Compared with the control group, the content of MDA in the tetrazole group was significantly higher than that in the control group (p0.01), the content of MDA in the erdostane group was lower than that in the pentylenetetrazol group (p0.01), but there was no significant difference between the two groups (p0.05). The results of 2.HE staining showed that the hippocampal neurons in the control group were closely arranged, with clear edges, clear cytoplasm, normal nuclear morphology and no necrotic neurons. In pentylenetetrazol group, the number of hippocampal neurons was scattered, the number of neurons was decreased, and a large number of necrotic neurons appeared in the shrinkage of the cell body and nucleus, and the necrotic neurons were found in the erdostam intervention group and sodium valproate group. There was significant difference between pentylenetetrazol group and control group (p0.01), and there was no significant difference between the two groups (p0.05). The positive expression of 3.BDNF: the staining intensity of pentylenetetrazol group was significantly higher than that of control group (p0.01), and the staining intensity of pentylenetetrazol group was lower than that of erdostam intervention group (p0.05). There was no significant difference between the treatment group and sodium valproate group (p 0.05). Conclusion: Erdostam can reduce the level of oxidative stress in hippocampus of epileptic rats. Preconditioning can not completely prevent the occurrence of epilepsy, but can reduce the degree of neuronal injury, suggesting the existence of neuroprotective effect. Erdostantan may be involved in neuronal protection by scavenging excess free radicals and increasing the expression of BDNF in hippocampus of pentylenetetrazol kindled rats.
【学位授予单位】：延边大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R742.1
本文编号：2421422
[Abstract]:Objective: to observe the changes of superoxide dismutase (SOD) activity, malondialdehyde (MDA) (MDA) content in hippocampus of epileptic model rats, the degree of neuronal pathological damage and the level of brain-derived neurotrophic factor (BDNF). To explore the possible mechanism of its antiepileptic effect. Methods: forty healthy male SD rats were divided into normal control group, pentylenetetrazol group, erdostam intervention group and sodium valproate group with 10 rats in each group. The epileptic seizures were induced by intraperitoneal injection of pentylenetetrazole, and pretreated by oral administration of 50mg/Kg and 100mg/Kg, respectively, in the Edostam intervention group and sodium valproate group. The activity of SOD and the content of MDA were measured in the right hippocampus, the distribution of BDNF positive cells in the left hippocampus was observed by immunohistochemistry, and the damage of hippocampal neurons was observed by HE staining. Results: 1. SOD activity and MDA level in hippocampus of rats: compared with control group, SOD activity in pentylenetetrazol group was significantly lower than that in control group (p0.01), and that in erdostam intervention group was higher than that in pentylenetetrazol group (p0.01), and that in erdostam intervention group was higher than that in pentylenetetrazol group (p0.01). There was no significant difference (p0.05). Compared with the control group, the content of MDA in the tetrazole group was significantly higher than that in the control group (p0.01), the content of MDA in the erdostane group was lower than that in the pentylenetetrazol group (p0.01), but there was no significant difference between the two groups (p0.05). The results of 2.HE staining showed that the hippocampal neurons in the control group were closely arranged, with clear edges, clear cytoplasm, normal nuclear morphology and no necrotic neurons. In pentylenetetrazol group, the number of hippocampal neurons was scattered, the number of neurons was decreased, and a large number of necrotic neurons appeared in the shrinkage of the cell body and nucleus, and the necrotic neurons were found in the erdostam intervention group and sodium valproate group. There was significant difference between pentylenetetrazol group and control group (p0.01), and there was no significant difference between the two groups (p0.05). The positive expression of 3.BDNF: the staining intensity of pentylenetetrazol group was significantly higher than that of control group (p0.01), and the staining intensity of pentylenetetrazol group was lower than that of erdostam intervention group (p0.05). There was no significant difference between the treatment group and sodium valproate group (p 0.05). Conclusion: Erdostam can reduce the level of oxidative stress in hippocampus of epileptic rats. Preconditioning can not completely prevent the occurrence of epilepsy, but can reduce the degree of neuronal injury, suggesting the existence of neuroprotective effect. Erdostantan may be involved in neuronal protection by scavenging excess free radicals and increasing the expression of BDNF in hippocampus of pentylenetetrazol kindled rats.
【学位授予单位】：延边大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R742.1
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