论文部分内容阅读
目的 探讨微量元素锌缺乏与胶质酸性纤维蛋白 ( GFAP)表达的关系及锌调节胶质细胞分化的机制。方法 给处于孕期及哺乳期的 ICR母鼠喂饲含不同锌水平饲料 ,采用 West-ern blot技术检测其仔代胚胎、大脑、小脑及肝组织中 GFAP的表达情况 ;同时在穿梭箱内检测成年仔鼠 ( 70日龄 )的学习能力 ;行为实验结束后 ,在仔鼠的海马脑片上进行诱导长时程增强 ( LTP)实验。结果 实验仔鼠小脑在新生期 (出生第 1天 ,P1 )开始表达 GFAP,而大脑在出生后第 5天( P5)才开始有 GFAP印迹出现 :之后至成年小脑及大脑持续表达 GFAP;实验鼠肝组织在发育全过程中均未见有 GFAP印迹。比较各实验组 GFAP表达量为 :P1至 P5期非缺锌组 ( 30 mg/kg及1 0 0 mg/kg) GFAP杂交条带明显强于缺锌组 ( 1 mg/kg及 5mg/kg) ;P1 0至成年期 ,缺锌组 ( 1 mg/kg及 5mg/kg)大脑及小脑 GFAP的杂交条带反而强于非缺锌组 ( 30 mg/kg及 1 0 0 mg/kg) ,其强度与膳食锌呈负依赖关系。行为学检测表明 ,轻度缺锌组 ( 5mg/kg)达到学会标准所需次数明显多于高锌组 ( 1 0 0 mg/kg) ;电生理检测表明 ,轻度缺锌组仔鼠海马脑片上诱导的 LTP明显低于高锌组上所诱导的。结论 补充锌在发育早期可促进神经前体细胞向神经胶质细胞分化及 GFAP表达 ;神经胶质细胞分化
Objective To investigate the relationship between trace zinc deficiency and the expression of glial fibrillary acidic protein (GFAP) and the mechanism of zinc regulating glial cell differentiation. Methods ICR female rats during pregnancy and lactation were fed diets containing different levels of zinc. The expression of GFAP in embryos, cerebrum, cerebellum and liver was detected by West-ern blot. The adult Pups (70 days old) learning ability; behavioral experiments after the offspring of rat hippocampal slices induced long-term potentiation (LTP) experiments. Results The cerebellum of experimental offspring began to express GFAP in the newborn (P1 on the first day of life), while GFAP in the brain began to appear on the 5th day after birth (P5): GFAP was continuously expressed in adult cerebellum and brain There was no GFAP blot in liver tissue during the whole process of development. GFAP expression in each experimental group was compared with that of GFAP in non-zinc deficient group (30 mg / kg and 100 mg / kg) from P1 to P5, which was significantly stronger than that of zinc deficient group (1 mg / kg and 5 mg / kg) (P <0.05) .From P1 0 to adulthood, the hybridization bands of GFAP in brain and cerebellum of zinc deficiency group (1 mg / kg and 5 mg / kg) were stronger than those of non-zinc deficiency group (30 mg / kg and 100 mg / kg) Intensity and dietary zinc was negatively dependent. Behavioral tests showed that the number of mild zinc deficiency group (5mg / kg) required to reach the standard was significantly higher than that of the high zinc group (100 mg / kg); electrophysiological examination showed that hippocampal The LTP induced on-chip was significantly lower than that induced on the high-zinc group. CONCLUSION: Zinc supplementation can promote the differentiation of neural precursor cells into glial cells and the expression of GFAP in the early stage of development. Glial cell differentiation