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目的:用改良多梗塞性脑痴呆(multi-infarct dementis,MID)模型,观察芍药苷对MID模型大鼠保护作用与路径,为开发神经原保护剂的候选化合物奠定药理学基础。方法:建立大鼠MID模型,观察剂量分别为20,10,5 mg·kg-1的芍药苷对MID大鼠的保护作用并观察行为学及认知功能,用免疫组织化学检测不同脑组织内Bcl-2,Bax蛋白表达,用HE染色和电镜观察大脑皮层及神经元结构变化。结果:假手术组无神经行为改变,与假手术组相比,MID模型组大鼠的苏醒时间、神经行为学评价、斜扳试验、学习记忆等认知功能障碍和脑组织神经元均受影响,与模型组相比,各用药组大鼠的苏醒时间、神经行为学评价、斜扳试验、学习记忆等认知功能障碍和脑组织神经元均有明显改善。结论:芍药苷可改变MID大鼠的神经行为,对大鼠MID模型有明显的改善作用,抑制Bax表达,促进Bcl-2的表达,有抗神经元凋亡的作用。
OBJECTIVE: To observe the protective effect and pathway of paeoniflorin on MID model rats by improving the model of multi-infarct dementis (MID), and to establish a pharmacological basis for the development of neuroprotectant candidate compounds. Methods: The rat model of MID was established. The protective effects of paeoniflorin at doses of 20, 10, and 5 mg · kg-1 were observed and the behavior and cognitive function were observed. Immunohistochemistry Bcl-2, Bax protein expression, the changes of cerebral cortex and neurons were observed by HE staining and electron microscopy. Results: Compared with sham operation group, the recovery time, neurobehavioral evaluation, oblique pull test, learning and memory impairment, and neuron in brain tissue of MID model group were all affected Compared with the model group, the recovery time, the neurobehavioral evaluation, the oblique pull test, learning and memory and other cognitive dysfunction and the neurons in brain tissue of rats in each group were significantly improved. CONCLUSION: Paeoniflorin can change the neurological behavior of MID rats, and can significantly improve the MID model of rats, inhibit the expression of Bax, promote the expression of Bcl-2, and prevent the apoptosis of neurons.