动物造模,脑缺血再灌注大鼠 z-bio 2021-11-04 728

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

　　Method: We used the middle cerebral artery occlusion (MCAO) method to establish a rat model of cerebral ischemia-reperfusion injury in SD rats. 40 SD male rats were randomly divided into sham operation group, model group (cerebral ischemia-reperfusion dysfunction group), astragaloside IV group and nimodipine group (positive drug group), and the other groups were reperfused for 2 hours. The intraperitoneal injection of astragaloside IV and nimodipine group was performed 24 hours after cerebral ischemia and 1 week before modeling. The ZeaLonga scoring method was used to detect the neuropathy of each group of rats, the TTC staining was used to detect the cerebral infarct volume, and the ELISA method was used to detect the inflammatory factor-tumor necrosis factor alpha (tumor necrosis factor alpha) in the brain tissue. α) and interleukins are detected. Detect the content of interleukin 1β (IL-1β) of 6 (IL-6), use Nistle staining to detect cerebral cortical nerve damage, and use transmission electron microscope to detect the ultrastructural changes of brain neurons.

　　Results: The rats in the sham operation group had normal nerve function, no cerebral infarction, abundant numbers of neurons and Nissl bodies, reasonable cell arrangement, and clear and normal cell structure. The neurological dysfunction of rats in the sham operation group and the model group was more serious, the number of cerebral infarction increased significantly (P\u003c0.05), and the inflammatory factors TNF-α, IL-6 and IL- content 1β were all increased (P\u003c0.05), the cell sequence is disturbed, the nucleus is deformed, impetigo, and the staining quality distribution becomes uneven. Compared with the model group, rats in the astragaloside IV group and nimodipine group had improved neurological function, decreased cerebral infarction volume (P\u003c0.05), and decreased TNF-α, IL-6 and IL content. -1β is significantly reduced (P\u003c0.05), the cells are arranged more neatly, the nucleus is 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. The mechanism may be related to the reduction of inflammation by astragaloside IV.