| 潘敏鸿,彭瑞云,高亚兵,等.高功率微波辐射后大鼠心脏β1肾上腺素能受体表达及其意义[J].中华放射医学与防护杂志,2006,26(3):298-300,287.PAN Min-hong,PENG Rui-yun,GAO Ya-bing,et al.Expression of β1-adrenergic receptor in rat heart irradiated with high power microwave[J].Chin J Radiol Med Prot,2006,26(3):298-300,287 |
| 高功率微波辐射后大鼠心脏β1肾上腺素能受体表达及其意义 |
| Expression of β1-adrenergic receptor in rat heart irradiated with high power microwave |
| 投稿时间：2005-06-27 |
| DOI： |
| 中文关键词: 高功率微波 心脏 β1肾上腺素能受体 免疫组织化学 RT-PCR |
| 英文关键词:High power microwave Heart β_ 1 -adrenergic receptor Immunohistochemistry RT-PCR |
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| 中文摘要: |
| 目的 探讨高功率微波(HPM)辐射后心脏β1肾上腺素能受体(β1-AR)表达的变化及其意义。方法 采用平均功率密度为50mW/cm2的S波段HPM模拟源辐射45只二级Wistar雄性大鼠,应用光镜、免疫组织化学、RT-PCR和图像分析技术,定量研究HPM辐照后大鼠心脏组织结构改变及β1-AR蛋白及mRNA变化规律。结果 50mW/cm2HPM辐射后大鼠心肌纤维排列紊乱,颗粒变性甚至肌浆凝聚,7d内进行性加重,14d后减轻;辐射后1d,β1-AR蛋白于心内膜下及肌层心肌细胞膜及胞浆表达增强,3d达高峰(P<0.05),7d仍有较强的表达(P<0.05),14d恢复至正常水平;β1-ARmRNA于6h～28d均见升高(P<0.01),除7d外,随时间延长,增强更加明显。结论 50mW/cm2的HPM辐射可造成心脏组织结构的损伤,心肌β1-AR表达增强,参与了HPM辐射致心脏损伤的病理生理过程。 |
| 英文摘要: |
| Objective To investigate the effect of high power microwave(HPM) radiation on the expression of β1-adrenergic receptor(β1-AR) in rat heart. Methods S-band HPM device with mean power density 50 mW/cm2 was used to radiate 45 healthy Wistar male rats. Light microscope, immunohistochemistry, reverse transcriptase polymerase chain reaction(RT-PCR) and image analysis were used to study the pathological characteristics of heart tissue and the expression of β1-AR on the protein and mRNA level. Results 50 mW/cm2 HPM radiation caused progressive cardiomyofilaments derangement, degeneration and sarcoplasm condensation within 7 d. β1-AR protein was increased in endocardium and myometrium, and reached a peak on 3 d(P<0.05) and returned to the normal level on 14 d. Transcription of β1-AR mRNA was upregulated in endocardium and myometrium, and peaked peaked on 6 h-28 d (P<0.01); the mRNA level progressively incresed with time since irradiation except on 7 d. Conclusion 50 mW/cm2 HPM radiation injured heart tissue and increase the expression of β1-AR playing an important role in the pathophysiology of heart injury induced by HPM. |
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