动物造模,脑缺血再灌注 z-bio 2022-07-08 381

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

　　Methods SD rats were used as experimental subjects, and the rat model of cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion (MCAO). 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). The cerebral ischemia group was given 2 hours of cerebral ischemia and then reperfused for 24 hours. The astragaloside IV group and the nimodipine group were given intraperitoneal injection one week before modeling. ZeaLonga scoring method was used to detect the neurological deficit of the rats in each group, TTC staining was used to detect the volume of cerebral infarction, and ELISA method was used to detect the inflammatory factors-tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) in brain tissue. 6) and interleukin-1β (IL-1β) content, Nissl staining was used to detect nerve cell damage in the cerebral cortex, and transmission electron microscopy was used to detect the ultrastructural changes of nerve cells in the cerebral cortex.

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

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