To investigate the neuronal losses of hens' spinal cords in the model of organophosphate-induced delayed neuropathy (OPIDN) and to analyze the impact of apoptosis on the pathogenesis of OPIDN. Adult hens were challenged with triorthocresyl phosphate (TOCP) at a single dose (750 mg/kg). Neuronal losses in the 3rd lumbar spinal cord (L3) were assessed by light-microscopy and electron-microscopy methods at different days post exposure, respectively. The typical OPIDN signs were seen in the TOCP-exposed hens at about 9th day. The number of large nerve cells declined gradually. And these cells were verified as neurons by immunostained with neuronal marker NeuN. The expression of FasL reached proximal at about 9th day, decreased from 14th day. Neurons in TOCP exposed groups displayed degenerative morphologies in electronic microscopy. Some neurons showed apoptotic-like ultrastructure profiles at 5th day. The nuclear membrane was complete with chromatin condensed to the margins of nuclear membrane like a crescent-shaped body. Mitochondria morphologic changes appeared early (5 d) following exposure to TOCP, and developed in a time-dependent fashion. Apoptosis might be involved in the development of OPIDN, and play a role in the pathogenesis of OPIDN.

译文

研究有机磷酸盐诱导的迟发性神经病 (OPIDN) 模型中母鸡脊髓的神经元丢失,并分析凋亡对OPIDN发病机理的影响。以单剂量 (750 mg/kg) 对成年母鸡进行磷酸三邻甲苯酯 (TOCP) 攻击。在暴露后的不同天,分别通过光学显微镜和电子显微镜方法评估了第三腰椎脊髓 (L3) 的神经元损失。在大约第9天,在暴露于TOCP的母鸡中可以看到典型的OPIDN迹象。大神经细胞的数量逐渐减少。通过用神经元标记NeuN免疫染色将这些细胞验证为神经元。FasL的表达在第9天左右达到近端,从第14天开始下降。TOCP暴露组的神经元在电子显微镜下显示出退化形态。某些神经元在第5天显示凋亡样超微结构。核膜是完整的,染色质浓缩到核膜的边缘,就像一个新月形的身体。暴露于TOCP后早期 (5 d) 出现线粒体形态变化,并以时间依赖性方式发展。凋亡可能参与OPIDN的发生发展,并在OPIDN的发病机制中起作用。

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