摘要
目的 观察锌与脑组织中 bcl- 2 m RNA表达关系 ,明确锌调节中枢神经系统发育及功能以及锌与神经细胞凋亡间的分子机制。方法 将成年刚怀孕 ICR雌性小鼠随机分为 5组并饲以不同锌水平的饲料 ,使其分别成为严重缺锌组 (1 mg/kg)、轻度缺锌组 (5mg/kg)、适锌组(30 mg/kg)、高锌组 (1 0 0 mg/kg)及高锌对喂组 (1 0 0 mg/kg)。实验动物在孕期和哺乳期均喂饲实验饲料 ,而断奶期 (2 0日龄 ,P2 0 )至成年 (70日龄 ,P70 )各组改喂普遍饲料。在 P2 0和 P70期收集各实验组动物脑组织 ,采用 Northern blot技术检测 bcl- 2 m RNA表达情况。结果 在 P2 0及 P70仔鼠脑组织中均有 bcl- 2 m RNA表达 ;P2 0期缺锌组 (严重缺锌组及轻度缺锌组 )实验仔鼠脑组织bcl- 2 m RNA的表达量明显少于非缺锌组 (适锌组、高锌对喂组及高锌组 ) ,并表现出与膳食锌水平呈正依赖关系 ;成年 (P70 )时 ,各实验组仔鼠脑组织 bcl- 2 m RNA表达水平未见明显差异。结论 锌对脑组织中神经细胞凋亡具有调节作用 ,发育期锌缺乏可促进脑细胞凋亡发生 ,并抑制 bcl- 2m RNA表达 ;补充锌可能通过提高 bcl- 2 m RNA转录水平抑制神经细胞凋亡。
Objective:To determine the molecular mechanisms of zinc on apoptosis, and on central nervous system development and function. Methods: Northern blot method was used to analyze the expression of bcl 2 mRNA in the brain of experimental offsprings on postnatal day 20 and 70 (P70, adult),whose dams were fed different zinc level diets (1 mg/kg,5 mg/kg,30 mg/kg and 100 mg/kg)during pregnancy and lactation respectively. Results:The results showed that the brain bcl 2 mRNA expression in zinc deficient groups (1 mg/kg and 5 mg/kg) was lower than that in zinc adequate group (30 mg/kg) and zinc supplemented group (100 mg/kg) on postnatal day 20. But there was no difference in brain bcl 2 mRNA expression among all experimental groups on postnatal day 70 (adult). Conclusion:The results suggest that zinc deficiency may induce apoptosis and inhibit bcl 2 mRNA expression of nervous cells during development, and zinc can regulate the expression of bcl 2 at transcription level and inhibit apoptosis by increasing bcl 2 expression.
出处
《营养学报》
CAS
CSCD
北大核心
2000年第2期105-108,共4页
Acta Nutrimenta Sinica
基金
国家自然科学基金! (39770 6 43)
全军九五医学科研规划第二批青年基金 !(98Q0 43)