摘要
目的:探讨新生鼠缺氧缺血性脑损伤(hypoxic-ischemic,HIE)脑组织谷氨酸、脑细胞内钙的改变及降钙素基因相关肽(calciumgene-relatedpeptide,CGRP)的神经保护作用,为临床治疗和早期康复提供理论依据。方法:实验于2003-05/09在广东医学院儿科实验室完成。选择45只7d龄SD大鼠,分为正常对照组、药物治疗组、生理盐水组。药物治疗组于HIE后给予CGRP3μg/(kg·d),腹腔内注射,连续3d,而生理盐水组每天给予同剂量生理盐水腹腔内注射。各组分别在规定时间内断头取脑。采用全自动氨基酸分析仪检测脑组织谷氨酸的浓度,应用钙荧光指示剂Fura-ZAM法测定脑细胞胞浆游离钙离子浓度。结果:新生鼠缺氧缺血后生理盐水组脑组织谷氨酸及细胞内钙浓度最高犤(2.83±1.39)μmol/L,(129.47±17.21)nmol/L犦,与正常对照组犤(1.45±0.56)μmol/L,(93.72±24.16)nmol/L犦比较差异有显著性意义(P<0.01),而药物治疗组犤(1.77±0.60)μmol/L,(103.35±12.46)nmol/L犦与正常对照组比较差异无显著性意义(P>0.05)。结论:CGRP能抑制缺氧缺血新生鼠脑组织谷氨酸的释放,从而阻止谷氨酸介导的钙内流,提示CGRP具有神经保护作用。
AIM: To study the protective role of calcium gene- related peptide (CGRP) in nerve and the changes of glutamic acid and free calcium in cells of hypoxic- ischemic (HIE) brain in neonatal rats to provide academic foundation for clinical treatment and early rehabilitation.METHODS: The experiment was finished in the Department of Pediatrics of Guangdong Medical College from May to September 2003. Forty- five SD rats of 7 days old were randomly divided into three groups: normal control group, CGRP group and saline group. In CGRP group, the rats were given CGRP intraperitoneal injection for 3 days in doses of 3 μ g/kg per day soon after the HIE model was performed. In saline group, the rats were given saline in same doses intraperitoneal injection for 3 days. All the rats were decapitated and the content of glutamic acid in cerebral tissue were detected with a full- automatic biochemical analyzer, and the concentration of dissociative calcium ion was measured with calcium fluorescence indicator in Fura- ZA.RESULTS: The contents of glutamic acid and free calcium ion in saline group [(2.83± 1.39)μ mol/L,(129.47± 17.21) nmol/L] were obviously higher than those in control group[(1.45± 0.56)μ mol/L,(93.72 ± 24.16)nmol/L] and there was significant difference(P< 0.01). But there was no significant difference in the content between control and CGRP groups[(1.77± 0.60) μ mol/L,(103.35± 12.46) nmol/L](P > 0.05).CONCLUSION: CGRP can inhibit the release of glutamic acid in hypoxic- ischemia cerebral cell and prevent calcium influx induced by glutamic acid, which may reveal CGRP has neural protective function.
出处
《中国临床康复》
CSCD
北大核心
2005年第9期60-61,共2页
Chinese Journal of Clinical Rehabilitation
基金
广东省湛江市科技攻关项目(020116)~~