【Abstract】Objective: To investigate the correlation between brain injury and spleen damage in rat models of acute ischemic stroke and stasis interaction, and its effect on the signal axis of MCP-1/CCR2 chemokine, and to provide experimental basis for the mechanism of "brain-spleen inflammatory coupling" in spleen lesions caused by acute ischemic stroke. Methods: Forty male SD rats were randomly divided into sham group, carrageenan/yeast stasis syndrome group (Carrageenan/Yeast, CA/Y), middle cerebral artery occlusion group (MCAO), middle cerebral artery occlusion (MCAO), middle cerebral artery stasis syndrome group (MCAO CA/Y), 10 rats in each group. The CA/Y group and the MCAO CA/Y group were injected with 10 mg穔g-1 carrageenan, 10 mg穔g-1 intraperitoneally on the first day of molding, and 2 mg穔g-1 of dry yeast suspension were injected subcutaneously on the second day, and the MCAO group and MCAO CA/Y group were established by wire embolism on the second day. 24 h after cerebral infarction model, the neurological deficit score was performed on each group of rats, the percentage of cerebral infarction area was observed by TTC staining, the spleen weight was determined, and the correlation between the percentage of cerebral infarction area and spleen weight was further analyzed by Spearman correlation coefficient, the pathological morphology of brain tissue and spleen tissue was observed by hematoxylin-eosin (HE) staining, and monocyte-1 (monocyte) was detected in rat plasma by enzyme-linked immunosorbent assay (ELISA). chemotactic protein 1, MCP-1), interferon-γ γ (IFN-γ) content, western blot method to detect ischemic side brain tissue chemokine C-C-motif receptor 2 (CCR2) protein expression. Results: Compared with the ham group, the neurological deficit score, cerebral infarction area, MCP-1 and IFN-γ content in plasma were significantly increased (P<0.01), spleen weight decreased significantly (P<0.01), and the expression of CCR2 protein in brain tissue was also significantly up-regulated (P<0.05) in the MCAO group and the MCAO CA/Y group. The area of cerebral infarction increased significantly (P<0.01), the weight of the spleen decreased significantly (P<0.01), and the expression of CCR2 protein in brain tissue and spleen tissue was also significantly up-regulated (P<0.05), compared with the MCAO group, the area of cerebral infarction in the MCAO CA/Y group was significantly increased (P<0.01) and the weight of the spleen decreased significantly (P<0.05). Spearman correlation analysis showed that spleen weight was negatively correlated with the percentage of cerebral infarction area (P<0.01, r=-0.9711). The pathological morphological observation results showed that the pathological changes in the MCAO CA/Y group were the most serious, cerebral liquefaction necrosis foci could be seen in the brain tissue cortex, the arrangement of neuronal cells in the lesions was sparse, disordered, volume atrophy, a small number of vacuoles and nuclear solidification, most of the neuronal cells were red degeneration and necrosis, microglia hyperplasia was obvious, small blood vessels were significantly increased, and interstitial lipid degeneration was superb; The density of periarterial lymph sheath cells in part of the spleen tissue is reduced, and the marginal area is widened. Conclusion: A correlation between brain and spleen injury could be found after acute ischemic stroke with stasis and toxins syndrome, and the chemokine signaling axis of MCP-1/CCR2 might be involved in the mechanism of "brain-spleen inflammation coupling".