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高同型半胱氨酸血症介导大鼠心肌Bcl-2、Bax基因甲基化的研究

侯建军1,贾绍斌2   

  1. 1. 宁夏医科大学
    2. 宁夏医科大学总医院心脏中心
  • 收稿日期:2012-09-27 修回日期:2012-12-03 出版日期:2013-04-15 发布日期:2013-04-15
  • 通讯作者: 贾绍斌

Hyperhomocysteinamia induce Bcl-2 and Bax methlation changes in rat's myocaidium

HOU Jian jun1,JIA Shao bing2   

  1. 1. Postgradulate College of Ningxia Medical University
    2. General Hospital of Ningxia Medical University，Ningxia 750004，China
  • Received:2012-09-27 Revised:2012-12-03 Published:2013-04-15 Online:2013-04-15
  • Contact: JIA Shao bing

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摘要：

【摘要】目的 观察高蛋氨酸灌胃诱导的高同型半胱氨酸血症（HHCY）大鼠模型中，HHCY对模型大鼠心肌组织Bcl-2、Bax启动子区DNA甲基化的影响。方法 选用22只5周龄健康雄性Wistar大鼠，随机分为对照组和HHCY 组，各11只；对照组给予普通大鼠饲料，HHCY组给予普通饲料加蛋氨酸1 g/（kg·d）灌胃，持续喂养20周后心脏取血，检测血清同型半胱氨酸（Hcy）浓度；提取心肌基因组DNA，甲基化特异性的PCR（MSP）联合巢式PCR检测大鼠心肌组织Bcl-2、Bax基因启动子区甲基化修饰状态的变化。结果20周蛋氨酸1 g/（kg·d）灌胃，可以诱导HHCY（P < 0.01）；与对照组比较，HHCY组大鼠心肌组织中Bcl-2启动子区呈高甲基化的改变[（1.28±0.02）vs（1.11±0.01）]，Bax启动子区呈低甲基化的改变[（0.80±0.01）vs（0.92±0.01）]，差异有统计学意义（t 分别为2.765和2.568，P < 0.01）。结论 HHCY 对心肌组织中Bcl-2、Bax甲基化的影响有差异，提示可能存在更深层次的机制。

关键词: 同型半胱氨酸, 高同型半胱氨酸血症, 基因, bcl-2, bcl-2相关X蛋白质, DNA甲基化, 大鼠, Wistar

Abstract:

[Abstract] Objective  To observe the effects of methionine-induced hyperhomocysteinamia (HHCY) on methylation status of myocardial B cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in rats. Methods  Twenty two healthy five-week-old male Wistar rats were randomly divided into control group and HHCY group (n=11 for each group). Rats were given ordinary food in control group. Rats were received ordinary food and methionine [1 g/(kg·d),orally] in HHCY group. Rats were sacrificed and blood samples were taken from heart of rats after 20 weeks. The serum homocysteine (Hcy) was detected with automatic biochemistry analyzer. Methylation-specific PCR and Nested PCR were used to examine methylation status of myocardial Bcl-2 and Bax. Results  The serum homocysteine was significantly higher in HHCY group than that of control group (P < 0.01). The hypermethylation happened in bcl-2 promoter region in HHCY group compared to that of control group (P < 0.05). The demethylation happened in Bax promoter region of HHCY group compared to that of control group (P < 0.01). Conclusion  The effects of HHCY on myocardial Bcl-2 and Bax methylation status are different，suggesting that there may be deeper mechanisms.

Key words: homocysteine, hyperhomocysteinemia, genes, bcl-2, bcl-2-associated X protein, DNA methylation, rats, Wistar