浓缩铀诱发新生大鼠发育脑损伤研究

来源 :苏州医学院学报 | 被引量 : 0次 | 上传用户:G715893600
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目的 研究浓缩铀 (2 3 5U)对Wistar纯品系新生大鼠发育脑的损伤效应。方法 通过建立脑辐射损伤的动物模型 ,运用 13种指标多方位探讨了2 3 5U辐照对新生大鼠体格生长及神经行为发育的影响 ;运用微观放射自显影示踪揭示2 3 5U在发育脑细胞中的行径动态 ;运用放射免疫技术检测2 3 5U在新生大鼠皮质、海马、间脑、小脑中神经元特异性烯醇化酶 (NSE)、白介素 - 1β(IL - 1β)、超氧化物歧化酶 (SOD)、内皮素 (ET)含量变化。 结果 2 3 5U脑内照射可使新生大鼠体重和脑重增长明显缓慢 ;在开眼时间、听觉惊愕、向亲性行为、游泳运动以及生理性反射如负趋地性、平面翻正、抓握反射、空中翻正均呈延迟 ,导致生长延缓及神经行为异常 ;观察微观放射自显影径迹发现 ,2 3 5U主要滞留在脑细胞核中 ,而在胞浆和细胞间隙中只有少量呈现 ;放射免疫检测表明 ,随着2 3 5U脑内照射剂量的增加 ,可使NSE含量下降 ,而IL - 1β却显著上升 ,而在低剂量2 3 5U脑内照射时 ,可诱导SOD和ET增升 ,在大剂量时却呈明显抑制。结论 浓缩铀 (2 3 5U)对发育脑损伤的作用特性具有神经细胞的敏感性和代偿性 Objective To study the effect of uranium enrichment (2 3 5 U) on brain development in neonatal rats with Wistar pure line. Methods The animal model of brain radiation injury was established and the effect of 2 3 5 U irradiations on the growth and neurobehavioral development of newborn rats was explored by using 13 indexes in different directions. The microscopic autoradiography tracing revealed that 23 U The neuronal specific enolase (NSE), interleukin - 1β (IL - 1β), superoxide dismutase (SOD) in the cortex, hippocampus, diencephalon and cerebellum of neonatal rats were detected by radioimmunoassay. Dismutase (SOD), endothelin (ET) content changes. Results Intracerebral irradiation of 23 5 U significantly slowed the growth of body weight and brain weight in newborn rats. In open eyes, arousals of consonance, swimming behavior and physiological reflex such as negative geotropism, Reflex, and skyward correction were delayed, resulting in growth retardation and neurobehavioral abnormalities. Observing microscopic autoradiography traces found that 235U mainly remained in the nuclei of the brain cells, while only a small amount appeared in the cytoplasm and intercellular space. Radioimmunoassay The results showed that with the increase of intracerebral irradiation dose of 23 5 U, the content of NSE decreased, but the level of IL - 1β increased significantly. However, the increase of SOD and ET could be induced when intracerebral irradiation of low dose High dose was significantly inhibited. Conclusions The effect of uranium enrichment (2 35 U) on the development of brain injury is characterized by the sensitivity and compensatory
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