Acta Anatomica Sinica ›› 2017, Vol. 48 ›› Issue (6): 642-650.doi: 10.16098/j.issn.0529-1356.2017.06.002

• Neurobiology • Previous Articles     Next Articles

 Nitrite exposure and DNA methylation and histone deacetylation in mouse brain

LIU Jun ZHANG Li-li SHI Zhen-yu* DENG Jin-bo*   

  1. Institute of Neurobiology, Nursing College, He’nan University, He’nan Kaifeng 475004, China
  • Received:2016-12-22 Revised:2017-02-18 Online:2017-12-06 Published:2017-12-06
  • Contact: DENG Jin-bo E-mail:jinbo_deng@henu.edu.cn

Abstract:

Objective To investigate the inflammatory damage in the mouse neocortex after nitrite exposure, and to understand the regulation mechanism of DNA methylation and histone deacetylation. Methods C57BL/6 J adult male mice were used to establish the models of prenatal nitrite exposure, wherefore control group (physiological saline), low dose nitrite exposure group (3 g/L) and high dose nitrite exposure group (6 g/L) were included. Immunocytochemistry and Western blotting were carried out to analyze the inflammatory damage, histone deacetylation and DNA methylation in the neocortex. Results The expressions of cyclooxygenase 2(COX2), interleukin-1β(IL-1β), ionized calcium binding adapor molecule-1(Iba1), c-Fos and IL-6 were significantly more than those in the control group (P<0.01) after chronic nitrite exposure. The expression of 5-methylcytosine(5-mC), DNA methyctrasferace 1(DNMT1), DNA DNMT3a and histone deacetylase 1(HDAC1) in treatment groups were significantly lower than that in the control group (P<0.01) with dose dependency. Conclusion Nitrite exposure can induce cell immune inflammatory damage in the neocortex of mice, and DNA methylation and histone deacetylation may be involved in regulation of immune inflammatory reaction after nitrite exposure.

Key words: Nitrite exposure, Inflammatory reaction, DNA methylation, Histone deacetylation, Western blotting, Mouse