| 魏丽,彭瑞云,高亚兵,王水明,马俊杰,徐新萍,苏镇涛,杨国山.高功率微波辐射后大鼠海马组织中突触后致密物-95及cAMP反应元件结合蛋白的变化[J].中华放射医学与防护杂志,2008,28(5):545-549 |
| 高功率微波辐射后大鼠海马组织中突触后致密物-95及cAMP反应元件结合蛋白的变化 |
| Changes in expressions of PSD-95 and CREB in hippocampi of rats after exposure to high power microwave |
| 投稿时间：2007-08-21 |
| DOI： |
| 中文关键词: 高功率微波辐射 海马 PSD-95 cAMP反应元件结合蛋白 |
| 英文关键词:High power microwave Hippocampus Postsynaptic density-95 Cyclic AMP-response element binding protein |
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| 中文摘要: |
| 目的 观察高功率微波(HPM)辐射后大鼠海马组织中突触后致密物(PSD)-95及cAMP反应元件结合蛋白(CREB)的变化。方法 采用10、30和100 mW/cm2 HPM照射75只Wistar雄性大鼠,于辐射后6 h、1、7、14和28 d活杀取海马组织,采用免疫组化、凝胶阻滞实验和图像分析等技术,观察海马神经元中PSD-95及CREB的变化。结果 HPM辐射后大鼠海马神经元胞浆中PSD-95的表达有不同程度的增加;10 mW/cm2组辐射后6 h, PSD-95表达增加,于辐射后1 d达高峰,28 d基本恢复正常;100 mW/cm2组辐射后6 h, PSD-95表达增加,MOD于1 d达高峰,IOD于7 d达高峰,28 d基本恢复至正常水平;30 mW/cm2组于辐射后3 d内,海马组织CREB与DNA的结合能力进行性降低。结论 HPM辐射后大鼠海马PSD-95表达增加,CREB与DNA结合能力减弱,参与了HPM辐射后海马组织损伤及海马神经元突触可塑性改变的病理生理过程。 |
| 英文摘要: |
| Objective To investigate the change of the expressions of PSD-95 and CREB in hippocampi of rats after exposure to high power microwave (HPM). Methods The HPM device with mean power densities of 10, 30 and 100 mW/cm2 was used to expose 75 healthy Wistar male rats, which were killed on at hour 6, days 1, 7, 14 and 28 after irradiation. The expressions of PSD-95 and CREB were analyzed by immunohistochemistry, gel retardation assay and imaging analysis. Results The expression of PSD-95 in hippocampi of rats was up-regulated after 10 and 100 mW/cm2 exposure. The levels of PSD-95 in hippocampi rised at hour 6 after exposure to 10 mW/cm2, peaked at day 1, and returned to the basal level at day 28 after exposure. The levels of PSD-95 went up at hour 6 after 100 mW/cm2 exposure, peaked at day 1 (MOD) and 7 (IOD) respectively, and returned to the basal level at day 28 after 100 mW/cm2
exposure. The binding ability of CREB and DNA was declined within 3 d after exposure to 30 mW/cm2 HPM. Conclusions The levels of PSD-95 in hippocampi are increased, but the binding ability of CREB and DNA declined after exposure to HPM, which is contributed to the patho-physiological process of hippocampus tissue injury. |
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