动物实验,黄芪甲苷,脑缺血再灌注 z-bo 2020-09-14 397

　　Objective To observe the effect of astragaloside IV on inflammatory factors and ultrastructure in rats with cerebral ischemia reperfusion.

　　Method Taking SD rats as experimental objects, the middle cerebral artery occlusion (MCAO) method was used to establish a rat model of cerebral ischemia-reperfusion injury. 40 SD male rats were randomly divided into sham operation group, model group (cerebral ischemia reperfusion injury group), astragaloside IV group and nimodipine group (positive drug group). Except for sham operation group, the rest Groups were reperfused for 24 hours after 2 hours of cerebral ischemia. Among them, the astragaloside IV group and the nimodipine group were injected intraperitoneally one week before modeling. ZeaLonga scoring method was used to detect neurological deficits in each group of rats, TTC staining was used to detect cerebral infarction volume, and ELISA method was used to detect inflammatory factors in brain tissue-tumor necrosis factor α (TNF-α) and interleukin-6 (IL- 6) And the content of interleukin-1β (IL-1β), Nissl staining was used to detect the neuronal damage in the cerebral cortex, and the transmission electron microscope was used to detect the ultrastructural changes of the neuronal cells in the cerebral cortex.

　　Results The nerve function of the rats in the sham operation group was normal, no cerebral infarction was found, the number of nerve cells and Nissl bodies were abundant, the cells were arranged neatly, and the cell ultrastructure was clear and normal. Compared with the sham operation group, the rats in the model group had neurological deficits More serious, the volume of cerebral infarction increased significantly (P<0.05), the contents of inflammatory factors TNF-α, IL-6, and IL-1β were all increased (P<0.05), the cell arrangement was disordered, the nucleus was deformed and pyknotic, and the chromatin distribution Uneven. Compared with the model group, the neurological function of the rats in the astragaloside IV group and the nimodipine group was improved, the cerebral infarction volume was reduced (P<0.05), and the contents of TNF-α, IL-6, and IL-1β were significantly decreased P< 0.05), the cells are arranged neatly, the nuclei are regular, and the chromatin distribution is more even.

　　Conclusion Astragaloside IV can inhibit cerebral ischemia-reperfusion injury in rats and improve the ultrastructural changes of nerve cells. Its mechanism may be related to astragaloside IV reducing inflammation.