Abstract

Background: Stroke is the first cause of death in Chinese residents. Plasminogen playes an important role in the process of anigiogenesis. But its specific mechanism of regulating angiogenesis after stroke is not clear. Method: We used wild-type (WT) mice and plasminogen knockout (KO) mice to conduct a permanent middle cerebral artery infarction model (MCAo). At different time points after operation we performed function test; used FITC to measure brain vascular distribution; used western-blot to detect the expression of TSP after MCAo. We used the cerebral vascular endothelial cells for tubeformation. All collected data were processed by corresponding image software, and the results were statistically analyzed by variance analysis or t test. Results: (1) The total length of capillary formation of cerebral vascular endothelial cells in group KO mice was less than that in group WT.(Figure 1) (2) The loss of motor sensory function in group WT was always less than that in group KO. (Figure 2) (3) After MCAo, the blood vessel density in the two groups of mice increased with time, and the density of blood vessels in the WT group was greater than that of the KO group. (Figure 3 ) (4) After MCAo, the levels of TSP-1 and TSP-2 in the cerebral tissue of KO and WT mice were higher than those in the contralateral brain. At the same time, the expression of TSP-1 and TSP-2 in the infarct lateral brain tissue of group KO was higher than that in group WT. (Figure 4) Conclusion: The lack of plasminogen can regulate the expression of TSP-1 and TSP-2 after ischemic stroke, thereby inhibiting the angiogenesis process of brain tissue after cerebral ischemia which leads to poor functional prognosis. stroke.

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