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甲醛对小鼠不同脑区的神经毒性作用

发布时间:2018-10-10 15:40
【摘要】:本研究旨在探讨甲醛导致机体神经系统病变的具体机制。选用雄性Balb/c小鼠为研究对象,动态吸入甲醛方式染毒7天,每天8 h,甲醛浓度分别为0、0.5、3.0 mg/m3,同时设置一氧化氮合酶(nitric oxide synthase,NOS)拮抗剂(NG-monomethylL-arginine,L-NMMA)组,该组小鼠同时进行3.0 mg/m3甲醛染毒。染毒结束后,用试剂盒检测小鼠大脑皮层、海马和脑干中环磷酸腺苷(cyclic adenosine monophosphate,cAMP)、环磷酸鸟苷(cyclic guanine monophosphate,cGMP)、一氧化氮(nitric oxide,NO)含量和NOS活性的变化。结果显示,与对照组相比,小鼠大脑皮层和脑干中cAMP含量在0.5 mg/m3染毒组显著升高(均P0.05),但是在3.0 mg/m3染毒组显著降低(P0.05),海马中cAMP含量仅在3.0 mg/m3染毒组出现显著降低(P0.05);与对照组相比,L-NMMA拮抗组小鼠cGMP和NO含量分别在海马和大脑皮层中显著上升(均P0.01),而cAMP含量和NOS活性在不同脑区中无显著变化。与3.0 mg/m3染毒组相比,L-NMMA拮抗组不同脑区中cAMP含量均显著上升(均P0.05),NOS活性显著下降(P0.05或P0.01);大脑皮层和脑干中的cGMP含量以及脑干中的NO含量亦出现显著性变化(P0.05或P0.01)。以上结果提示,甲醛暴露的神经系统毒性作用与NO/cGMP信号转导通路和cAMP信号通路存在一定的关系。
[Abstract]:The purpose of this study was to explore the mechanism of formaldehyde causing neuropathy. Male Balb/c mice were exposed to formaldehyde for 7 days and 8 hours a day. The concentration of formaldehyde was 0.5 mg/m3, and 3.0 mg/m3, respectively. The mice were treated with (nitric oxide synthase,NOS antagonist (NG-monomethylL-arginine,L-NMMA). The mice were exposed to 3.0 mg/m3 formaldehyde at the same time. After exposure, the changes of (cyclic adenosine monophosphate,cAMP, (cyclic guanine monophosphate,cGMP, nitric oxide,NO and NOS activity in cerebral cortex, hippocampus and brainstem of mice were detected by using the kit. The contents of cyclic guanosine monophosphate (cyclic guanine monophosphate,cGMP) and the content of cyclic adenosine monophosphate (nitric oxide,NO) in hippocampus and brain stem were measured. The results showed that, compared with the control group, The content of cAMP in cerebral cortex and brainstem of mice increased significantly at 0.5 mg/m3 (P0.05), but decreased significantly in 3.0 mg/m3 group (P0.05), and cAMP content in hippocampus decreased only in 3.0 mg/m3 group (P0.05). Compared with control group, L-NMMA antagonistic group was smaller than control group. The contents of cGMP and NO increased significantly in hippocampus and cerebral cortex respectively (P0.01), but the content of cAMP and the activity of NOS did not change in different brain regions. Compared with 3.0 mg/m3 group, cAMP content in different brain regions of L-NMMA antagonistic group increased significantly (P0.05 or P0.01), and cGMP content in cerebral cortex and brainstem and NO content in brainstem also showed significant changes (P0.05 or P0.01). These results suggest that the neurotoxicity of formaldehyde exposure is related to NO/cGMP signal transduction pathway and cAMP signaling pathway.
【作者单位】: 华中师范大学生命科学学院遗传调控与整合生物学湖北省重点实验室;
【基金】:supported by the Key Project of National Natural Science Foundation of China(No.51136002) the Open Project Program of Hubei Key Laboratory of Genetic Regulation and Integrative Biology,China(No.GRIB201501)
【分类号】:R114

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