摘要
目的研究母体免疫球蛋白G(immunoglobu lin G,IgG)对N甲基D天冬氨酸(N-m ethyl-D-aspartate,NMDA)诱导的其幼鼠海马神经元损伤的作用及机制。方法通过体外幼鼠海马神经元原代培养,观察海马神经元在NMDA神经毒性作用下的变化,以及给予不同浓度的母体IgG后的影响。通过测定神经元漏出的乳酸脱氢酶(lactic dehydrogenase,LDH)活力,观察神经元损伤情况,用锥虫蓝染色观察细胞死亡率。结果体外神经毒性损伤后,培养神经元漏出的LDH较NMDA处理前和正常对照组高(P<0.01);给予不同浓度的母体IgG(分别为10 mg/L、100 mg/L)后,LDH漏出较NMDA组低(均P<0.01),而且较大剂量比小剂量的保护作用更为显著(P<0.05)。锥虫蓝染色显示NMDA组神经元死亡率较NMDA处理前和正常对照组高(P<0.01);给予不同浓度的母体IgG(分别为10 mg/L、100 mg/L),死亡率均比NMDA组低(P<0.05、0.01),而且较大剂量比小剂量的保护作用更强(P<0.05)。结论体外幼鼠海马神经元原代培养结果表明,50μmol/L NMDA可诱导幼鼠海马神经元损伤,母体IgG对NMDA的神经毒性有保护性作用,而且有剂量依赖关系。
Objective To investigate possible protective effect of maternal immunoglobulin G（IgG） against N-methyl-D-aspartate-mediated neurotoxicity on primary-cultured rat hippocampal neurons and the mechanism of the effect. Methods An in vitro system had been developed for the study of hippocampal neurons. Intracellular lactic dehydrogenase （LDH） release was used as a marker to measure the rates of neuronal damage. The cells were stained with Trypan blue to measure the rate of neuronal death. Results N-methyl-D-aspartate（NMDA） at a concentration of 50 μmol/L resulted in increased release of LDH and the cell mortality（ P 〈 0. 01, respectively）. Maternal IgG of different concentration （ 10 rag/L, 100 rag/L） inhibited NMDA-induced intracellular LDH release （ P 〈 0. 01, respectively） and cell mortality （ P 〈 0. 05, 0. 01, respectively）, and larger dose had stronger effect （P 〈 0. 05 ）. Conlusions Maternal IgG had protective effect on primary-cultured rat hippocampal neurons injured by NMDA and the effect was dose- dependent.
出处
《中华儿科杂志》
CAS
CSCD
北大核心
2006年第5期374-376,共3页
Chinese Journal of Pediatrics
基金
北京市自然科学基金资助项目(7042024)
