谷氨酸受体抗体诱导海马神经元损伤的研究

Anti-GluR3 Antibody Induces Injury of Hippocampal Neuron in Vitro

目的:有研究发现谷氨酸受体(GluR)与难治性癫的发作相关,故研究GluR亚单位抗体(GluR3抗体)对海马神经元的损伤作用。方法:取SD新生鼠海马皮质组织,以此培养的原代海马神经元作为靶细胞。抗体在不同的作用时间(20和40h)和稀释倍数下,通过细胞存活率(MTT法)和乳酸脱氢酶(LDH)释放量来测定抗体对神经元的毒性;TUNEL染色法测定神经元的凋亡。结果:GluR3抗体对神经元具有细胞毒性和凋亡作用,并与抗体的滴度和作用时间呈剂量依赖性。即使在低滴度的情况下(×1000和×2000),此抗体仍可诱导凋亡,且与对照组比较差异有显著统计学意义(P<0.01,P<0.05)。结论:GluR3抗体的致机制可能与其能诱导神经元的损伤有关。

Many reports indicated that autoantibodies to glutamate receptor （GluR） were correlated with intractable seizure. This paper would investigate injury of neuron induced by anti-GluR3 antibody. Methods： Original hippocampal neurons, from hippocampal cortex of neonatal SD rat, were cultured and were as a target cell. Anti-GluR3 antibody was carried out at two time-windows （20 h and 40 h） and at different dilutions. The survival rate of neuron （used MTT method） and the release of lactate dehydrogenase （LDH） were used to evaluate cytotoxicity, and TUNEL staining was applied to apoptosis of neuron. Results： Anti-GluR3 antibody could induce both cytotoxicity and apoptosis on original hippocampal neuron, which were concentration-dependent and time-dependent. Even though under low titer （ × 1 000 or × 2 000）, anti-GluR3 antibody could induce apoptosis, which is significantly higher than that in control group （P 〈 0.01 or P 〈0.05 ）. Conclusion： The mechanism of anti-GluR3 antibody involved epilepsy may be links to injury of neuron.