右美托咪定对谷氨酸诱导的大鼠神经系统毒性作用的影响

发布时间：2019-05-05 20:56

【摘要】：目的探讨右美托咪定(Dex)对大鼠谷氨酸神经毒性作用的影响及其机制。方法采用脑室注射谷氨酸制作大鼠脑谷氨酸神经毒性模型,将36只SD大鼠随机分为对照组(C组)、谷氨酸损伤组(G组,脑室注射谷氨酸)、Dex1组(脑室注射谷氨酸前30 min腹腔注射Dex 50μg/kg)和Dex2组(脑室注射谷氨酸前30 min腹腔注射Dex 100μg/kg)。2 h后取脑,分离出右侧海马组织测定超氧化物歧化酶和丙二醛,剩余脑组织测定脑含水量。另用尼氏染色法检测神经细胞受损状态。结果 Dex1组和Dex2组的脑组织含水量、丙二醛水平比G组明显降低,超氧化物歧化酶明显升高。同G组相比,Dex1组、Dex2组海马尼氏染色结果显示神经细胞损伤减轻明显。结论 Dex预处理可以明显减轻谷氨酸介导的神经毒性作用,其机制可能是通过增加超氧化物歧化酶,抑制氧化应激反应从而拮抗谷氨酸引起的细胞神经毒性作用。
[Abstract]:Objective to investigate the effect and mechanism of (Dex) on glutamate neurotoxicity in rats. Methods the rat brain glutamate neurotoxicity model was established by intracerebroventricular injection of glutamic acid. 36 SD rats were randomly divided into control group (group C), glutamic acid injury group (group G, intraventricular injection of glutamic acid). Dex1 group (intraventricular injection of Dex 50 渭 g / kg 30 min before intracerebroventricular injection) and Dex2 group (intraventricular injection of Dex 100 渭 g / kg). 30 min before intracerebroventricular injection) were taken 2 hours later to separate the right hippocampal tissue for determination of superoxide dismutase (SOD) and malondialdehyde (MDA). The residual brain tissue was measured for brain water content. Nissl staining was used to detect the damaged state of nerve cells. Results the water content, malondialdehyde (MDA) and superoxide dismutase (SOD) of brain tissue in Dex1 group and Dex2 group were significantly lower than those in G group. Compared with G group, the results of Haimi's staining in Dex1 group and Dex2 group showed that the injury of nerve cells was alleviated obviously. Conclusion Dex pretreatment can reduce the neurotoxicity induced by glutamic acid. The mechanism may be to antagonize the neurotoxicity induced by glutamate by increasing superoxide dismutase and inhibiting oxidative stress.
【作者单位】：中国医科大学附属盛京医院麻醉科;
【基金】：国家自然科学基金(81271370)
【分类号】：R614

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