维生素B_(12)及其衍生物甲钴胺对低糖导致的视网膜神经元损伤的保护作用  

Neuroprotective effects of vitamins B_(12) and its analog methylcobalamin on the hypoglycemia injured retinal neurons in vitro

作　　者：白海青[1] 王竫华[1] 李树宁[1] 张蕊石[1] 

机构地区：[1]青岛大学医学院附属医院眼科,山东青岛266003

出　　处：《眼科新进展》2003年第4期239-241,共3页Recent Advances in Ophthalmology

摘　　要：目的 评价维生素B_(12)及其衍生物甲钴胺对低糖导致的视网膜神经元损伤的保护作用。方法 新生大鼠视网膜单细胞悬液接种到细胞培养板中。低糖(葡萄糖浓度为0.56mmol·L^(-1))处理的同时加入不同浓度的维生素B_(12)和甲钴胺,继续培养至第4天,用四唑盐微量比色法检测细胞活力,细胞损伤程度用乳酸脱氨酶释放量进行评价。对数据进行统计分析。结果 低糖处理组与未处理组相比,视网膜神经元活力显著下降(P<0.01);甲钴胺浓度为0.5～1.0μmol·L^(-1)时,用药组视网膜神经元活力明显高于未加药组(P<0.05;P<0.01);维生素B_(12)在0.5～1.5μmol·L^(-1)时对低糖损伤的视网膜神经元活力无明显影响。维生素B_(12)和甲钴胺在1.0μmol·L^(-1)时均能够有效抑制低糖损伤引起的乳酸脱氢酶释放。如果低糖处理后才开始应用维生素,则各用药组均无明显神经保护作用。结论 维生素B_(12)和甲钴胺在一定药物浓度时对低糖引起的视网膜神经元损伤有保护作用,并且甲钴胺的神经保护作用高于B_(12)。低糖损伤后延迟给药则未发现其神经保护作用。Objective To evaluate the neuroprotectivity of vitamin B12 and its analog methylcobalamin, and their efficient concentrations on the glucose deprived retinal neurons. Methods Neonatal rat retinal neuron suspensions were planted on 96 well cell culture plates. After 24 hours in vitro culture, the cultures were glucose deprived for 6 hours. Certain concentrations of vitamin B12 and methylcobalamin were applied simultaneously at the beginning or just after the insult, and the non-neurons were inhabited at the same time. Continued culturing with vitamin B12 and methylcobalamin were given until the 4th day, then monotetrazolium(MTT)chromatometry was applied to assess the viability of retinal neurons. Lactate dehydrogenase(LDH)releasing were detected to evaluate the injury of retinal neurons. The data were analysed statistically. Results The viability of retinal neurons dropped significantly after glucose deprivation insult versus non-treating cultures (P < 0. 01). Methylcobalamin effectively inhibited the decreasing of cell viability in their concentration of 0.5-1.0mol L-1(P<0.01). Vitamin B12 didn' t affect the viability of retinal neurons. Among 0.5-1. Sfimol'L^ 'LDH releasing showed both vitamin B12 and methylcobalamin could effectively protect retinal neuons from damage in their concentration of 1.0mol L-1. Furthermore, both drugs exhibit weak efficiency of neuroprotection when they are used after hypoglycemia insult instead of simultaneously. Conclusion Vitamin 612 and its analog are able to demonstrate their protection on glucose deprived retinal neurons when acquiring certain concentrations, and methylcobalamin is more efficient than vitamin B12. However, delayed supplying of this drug will not significantly save the retinal neurons from hypoglycemia injuring. Vitamin B12 shows no obvious neuroprotection on in vitro rat retinal neurons in this study.

关 键 词：视网膜神经元 低糖 保护 维生素B12 甲钴胺 

分 类 号：R338[医药卫生—人体生理学] R774[医药卫生—基础医学]