天津医药 ›› 2015, Vol. 43 ›› Issue (11): 1281-1283.doi: 10.11958/j.issn.0253-9896.2015.11.016

• 实验研究 • 上一篇    下一篇

生长期膳食缺锌小鼠肾细胞凋亡及机制研究

田娟, 郭芳, 李晓明   

  1. 辽宁医学院组织学与胚胎学教研室 (邮编 121001
  • 收稿日期:2015-04-23 修回日期:2015-05-28 出版日期:2015-11-15 发布日期:2015-11-15
  • 通讯作者: 田娟 E-mail:tian555juan555@sina.com
  • 作者简介: 田娟 (1976), 女, 博士, 硕士研究生导师, 主要从事肾脏发育生物学研究
  • 基金资助:
    辽宁省科学技术计划项目 (2013022067); 辽宁省教育厅科学技术研究项目 (L2012307); 辽宁省大学生创新创业训练计划项目
    201410160037); 国家级大学生创新创业训练计划项目 (201410160037); 辽宁省高等学校优秀人才项目 (LJQ2013092

Study on the mechanism of apoptosis of mouse kidney cells in dietary zinc deficiency during the growth period

TIAN Juan,  GUO FangLI Xiaoming   

  1. Department of Histology and Embryology, Liaoning Medical College, Jinzhou 121001, China
  • Received:2015-04-23 Revised:2015-05-28 Published:2015-11-15 Online:2015-11-15
  • Contact: TIAN Juan E-mail:tian555juan555@sina.com

摘要: 目的 观察膳食缺锌条件下生长期小鼠肾细胞凋亡情况、 氧化应激情况及凋亡相关因子 Bcl-2 Bax 表达变化, 探讨锌缺乏诱发肾细胞凋亡的机制。方法 将刚断乳雄性小白鼠 30 只随机分为缺锌组和足锌组, 每组15 只。缺锌组喂饲缺锌饲料(0.85 mg/kg), 足锌组喂饲足锌饲料 (30 mg/kg)。应用 TUNEL 法观察小鼠肾细胞凋亡情况, 计算凋亡指数; 分别应用黄嘌呤氧化酶法和硫代巴比妥酸法测定肾超氧化物歧化酶 (SOD) 和丙二醛(MDA)含量;应用蛋白印迹技术检测肾组织中 Bcl-2Bax 蛋白表达变化。结果 与足锌组比较, 缺锌组小鼠肾可见 TUNEL 阳性细胞增多, 细胞凋亡指数明显增加; 抗氧化酶 SOD 活性下降, MDA 增加, 氧化应激反应增强; 凋亡相关因子 Bcl-2 白表达量明显下降, Bax 蛋白表达量明显上调, Bcl-2/Bax 比值下降。结论 生长期膳食缺锌导致肾细胞抗氧化酶活性降低, 氧化应激反应增强及细胞凋亡相关因子 Bcl-2 和 Bax 蛋白表达改变, 最终导致肾细胞发生凋亡。

关键词: 锌, 细胞凋亡, 肾, 氧化性应激, bcl-2 相关 X 蛋白质, 缺锌

Abstract: Objective To observe the cell apoptosis, oxidative stress reaction and expressions of Bcl-2 and Bax in kidney of dietary zinc deficiency mice during growth period, and discuss the mechanism of renal cell apoptosis induced by zinc deficiency. Methods Thirty weaning male mice were randomly divided into zinc-deficient group and zincadequate group, and 15 mice for each group. Zinc-deficient group was fed with zinc deficiency diet (0.85 mg/kg), while zinc-adequate group was fed with enough zinc diet (30 mg/kg). The TUNEL method was applied to observe the cell apoptosis, and the apoptotic index was measured. The content of SOD and MDA were detected to observe the oxidative stress reaction in kidney. The expression levels of Bcl- 2 and Bax protein were detected by Western blot assay. Results Compared with zinc- adequate group, the cell apoptosis and oxidative stress reaction were increased in zinc-deficient group. The expression of Bcl- 2 decreased, and the expression of Bax increased. The ratio of Bcl-2 and Bax declined in kidney of zinc deficiency mice. Conclusion Diet zinc deficiency in growth period may result in the decreased antioxidase, the increased oxidative stress reaction, and the changed Bcl-2 and Bax expression, which promote the occurrence of cell apoptosis in kidney.

Key words: zinc, apoptosis, kidney, oxidative stress, bcl-2-associated X protein, zinc deficiency