光化学反应法建立拟血管性痴呆大鼠模型的改进

A Rat Model of Vascular Dementia by Photochemical Induction

目的建立拟血管性痴呆大鼠模型,以期为血管性痴呆病理研究和防治药物开发提供可靠实用的动物模型。方法利用光化学反应诱导血栓形成的原理,短时间内造成大鼠脑皮质完全性局灶性梗死,7 d后测定其水迷宫学习记忆与空间探索能力;电镜观察神经细胞、突触形态结构;免疫组化染色观察神经细胞Fas表达。结果模型组大鼠学习记忆与空间探索能力下降,与对照组和生理盐水组比较差异有显著性(分别为P<0.05,P<0.01);电镜下,模型组大鼠出现神经细胞核内染色质固缩、边聚、断裂等凋亡征象,突触数量减少且结构破坏,神经髓鞘水肿;模型组大鼠神经细胞Fas表达与其他两组比较显著增多(P<0.01)。结论光化学反应法建立的拟血管性痴呆大鼠模型在神经细胞超微结构、FAS免疫组化染色等方面具有血管性痴呆部分临床病理特征。

Objective Set up a rat model of vascular dementia （VD）, for pathological investigation on VD to improve clinical treatment. Methods A rat model of VD was set up with blood stasis by photochemical induction was tested through place test and spatial probe test, observing the structure of neuron and synapse under the electron microscope, with immunohistochemical for FAS expression on neurons. Results The rats in model group were in lower potency to learn and memory, there was significant difference between the rats in model group and those in control groups （P〈0. 05,0. 01）. Under the electron microscope, the chromosomes of model rats neuron was broken and clustered near the nucleus membrane. It was also observed that the number of synapses in the cortex of model rats was significantly decreased and the structure of neuron was damaged. The expression of FAS in model rats neuron was stained stronger than those in control groups. Conclusions The VD model rat set up by photochemical reaction has pathological characters in the brain, both in neuron ultrastructure and FAS immunosraining.