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目的探讨长期噪声暴露对大鼠海马的影响及其机制。方法 24只雄性SD大鼠分为对照组与噪声暴露组(100 dB,白噪声,4 h/d×30 d),检测噪声暴露组动物中海马的N-甲基-D-天冬氨酸受体2B亚基(NR2B)的表达和tau蛋白的磷酸化状态;为了探讨其可能机制,用DNA断裂原位末端标记法检测海马神经细胞凋亡状态。结果长期噪声暴露后,实验组与对照组相比海马中NR2B的表达下降达41%,tau蛋白发生过度磷酸化的程度升高2.1倍和海马神经细胞凋亡数量占总神经元细胞数量的0.5%～1%;免疫组织化学结果显示海马中tau蛋白发生过度磷酸化的区域主要在齿状回(DG)区和安蒙氏角(CA)1区。结论长期噪声暴露引起大鼠神经递质系统异常及tau蛋白过度磷酸化可能诱发神经细胞凋亡和认知障碍。
Objective To investigate the effects of long-term noise exposure on hippocampus of rats and its mechanism. Methods Twenty-four male Sprague-Dawley rats were randomly divided into control group and noise exposure group (100 dB, white noise, 4 h / d × 30 d). The hippocampal N-methyl-D-aspartate Receptor 2B subunit (NR2B) expression and phosphorylation status of tau protein. To explore its possible mechanism, apoptotic status of hippocampus neurons was detected by DNA fragmentation in situ end-labeling. Results After prolonged noise exposure, the expression of NR2B in the hippocampus was decreased by 41% in the experimental group compared with that in the control group. The degree of hyperphosphorylation of tau protein was increased 2.1-fold and the number of apoptotic neurons in the hippocampus was 0.5 % ~ 1%. Immunohistochemistry showed that hyperphosphorylation of tau in the hippocampus was mainly located in the DG region and the Angstrom (CA) region 1. Conclusion Long-term noise exposure may cause abnormal neurotransmitter system and hyperphosphorylation of tau in rats, which may induce neuronal apoptosis and cognitive impairment.