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目的从一氧化氮神经递质角度探讨母源性BDE-209损伤仔鼠神经系统的可能机制。方法 3月龄wistar雌鼠自确定交配成功后随机分为实验组A、B、C、D和对照组E,通过胃灌方法建立自妊娠期至哺乳期的不同剂量BDE-209(100、300、600、1200mg/kg/d)的暴露模型,21天仔鼠断乳后各组随机选取10只仔鼠作为研究对象,应用光电比色法和放射免疫法分别测定各组仔鼠海马组织中一氧化氮(NO)含量、神经元型一氧化氮合成酶(nNOS)活性、环鸟苷酸(cGMP)含量。结果与对照组E相比,C、D组NO含量和nNOS活性明显增加(P<0.05);B、C、D组cGMP含量明显升高(P<0.05)。结论一定剂量的母源性BDE-209可能通过影响仔鼠NO神经信号递质系统影响其神经认知功能。
OBJECTIVE: To explore the possible mechanism of neurotoxicity in the offspring of maternal BDE-209 injured rats from the point of view of nitric oxide neurotransmitter. Methods Three-month-old female wistar mice were randomly divided into experimental groups A, B, C and D and control group E after successful mating. Eighteen different doses of BDE-209 (100, 300 , 600,1200 mg / kg / d). After 21 days of offspring weaning, 10 offspring were randomly selected from each group as study object. The changes of hippocampal formation in hippocampus of each group were detected by photometric colorimetry and radioimmunoassay Nitric oxide (NO), neuronal nitric oxide synthase (nNOS) activity and cyclic guanosine monophosphate (cGMP) were measured. Results Compared with the control group, the levels of NO and nNOS in group C and group D increased significantly (P <0.05). The levels of cGMP in groups B, C and D increased significantly (P <0.05). Conclusion A certain dose of maternal BDE-209 may affect its neurocognitive function by affecting NO neurotransmitter system in offspring.