小鼠大脑亚硝酸盐暴露与DNA甲基化和组蛋白去乙酰化

发布时间：2018-03-17 16:28

  本文选题：亚硝酸盐暴露　切入点：炎症反应　出处：《解剖学报》2017年06期 　论文类型：期刊论文

【摘要】：目的观察慢性亚硝酸盐暴露对小鼠大脑皮质炎症损伤的影响及其探讨DNA甲基化和组蛋白去乙酰化等相关机制。方法选取8周龄健康雄性C57BL/6J小鼠,随机分为对照组(生理盐水)、低剂量亚硝酸盐组(3g/L)和高剂量亚硝酸盐组(6 g/L),建立亚硝酸盐暴露模型,收集各组小鼠大脑皮质,利用免疫荧光染色法和Western blotting法分析大脑皮质炎症损伤,组蛋白去乙酰化酶和DNA甲基化相关酶的表达情况。结果慢性亚硝酸盐暴露后小鼠大脑皮质炎症损伤因子环氧化酶2(COX2)、白细胞介素-1β(IL-1β)、离子钙接头蛋白分子1(Iba1)、c-Fos、IL-6表达量明显多于对照组(P0.01),同时高剂量暴露组DNA甲基化相关酶5-甲基胞嘧啶(5-m C)、DNA甲基转移酶1(DNMT1)、DNMT3a、和组蛋白去乙酰化酶1(HDAC1)表达明显低于对照组(P0.01)且都呈亚硝酸盐剂量依赖性。结论亚硝酸盐暴露可通过促进细胞免疫炎症对小鼠大脑皮质造成损伤,并且DNA甲基化和组蛋白去乙酰化可能参与了慢性亚硝酸盐暴露过程中的应答过程及其调控机制。
[Abstract]:Objective to observe the effects of chronic nitrite exposure on inflammatory injury of cerebral cortex in mice and to explore the mechanisms of DNA methylation and histone deacetylation. Methods healthy male C57BL / 6J mice aged 8 weeks were selected. The rats were randomly divided into control group (normal saline group, low dose nitrite group) and high dose nitrite group (6 g / L) to establish nitrite exposure model and collect cerebral cortex of each group. The inflammatory injury of cerebral cortex was analyzed by immunofluorescence staining and Western blotting method. The expression of histone deacetylase and DNA methylation related enzymes. Results after chronic nitrite exposure, the expression of cyclooxygenase 2 (COX2), interleukin-1 尾 (IL 1 尾), ion calcium junction protein molecule 1 (IBA 1) and c-Fossin-6 (IL-6) in the cerebral cortex of mice exposed to chronic nitrite were detected. The expression of 5-methylcytosine 5-methylcytosine 5-methylcytosine (5-methylcytosine 5-methylcytosine 5-methylcytosine) and histone deacetylase (1HDAC1) in high dose exposure group was significantly lower than that in control group (P 0.01) and the expression of DNMT3a and histone deacetylase 1HDAC1 was significantly lower than that in control group (P 0.01) and the expression of DNMT3a and histone deacetylase 1HDAC1 was significantly lower than that in control group (P 0.01). It is suggested that nitrite exposure may damage the cerebral cortex of mice by promoting cellular immune inflammation. DNA methylation and histone deacetylation may be involved in the response process and its regulatory mechanism during chronic nitrite exposure.
【作者单位】： 河南大学护理学院河南大学神经生物研究所;
【基金】：河南省高等学校重点科研项目(15A180031,16A330001)
【分类号】：R99
，

本文编号：1625558