Acta Anatomica Sinica

AAS ›› 2015, Vol. ›› Issue (3): 289-196.doi: 10.16098/j.issn.0529-1356.2015.03.001

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Effects of prenatal nitrite exposure on hippocampus of mouse pups

HU Sang CUI Zhan-jun GUO Jun-nan LIANG Shuang YAN Ming-chao DENG Jin-bo* DENG Jie-xin*   

  1. Institute of Neurobiology, Nursing College, He’nan University, He’nan Kaifeng 475004, China
  • Received:2014-12-08 Revised:2015-01-19 Online:2015-06-06 Published:2015-06-06
  • Contact: DENG Jin-bo, DENG Jie-xin E-mail:jinbo_deng@henu.edu.cn

Abstract:

Objective To investigate the effects on hippocampus after prenatal nitrite exposure. Methods C57BL/6J mice were used to establish the models of prenatal nitrite exposure with control group (physiological saline), low dose nitrite exposure group (60 mg/kg) and high dose nitrite exposure group (120mg/kg). The pups of different groups at P0, P7, P14 and P30 were gathered for immunofluorescence, comet assay and Western blotting analysis to detect the hippocampal injury. Results In both nitrite exposure group and control group, the number of proliferative neuron in dentate gyrus gradually decreased with the growing age. At postnatal day 0 (P0), P7, P14 and P30, after prenatal nitrite exposure, 5-bromo-2-deoxy Uridine (BrdU) positive cells decreased with dose dependency (P<0.05, n=96). In order to identify if the inhibtion was selective, we observed BrdU positive cells in subventricular zone (SVZ) at P0 mouse. After nitrite exposure, BrdU positive cells in SVZ also decreased with dose dependency (P<0.05). The inflammatory injury and apoptosis cells in hilus increased with dose dependency after nitrite exposure (P<0.05). The tail of hippocampus cells in nitrite exposure groups was longer than that in control groups with dose dependency (P<0.01). The expressions of Caspase-8 and nuclear factor κB (NF-κB) protein in nitrite exposure groups in hippocampus were much higher than that in control groups (P<0.05). Conclusion Prenatal nitrite exposure can induce various hippocampus injuries, such as neuroproliferative inhibition, oxidative stress and neuroapoptosis.