动物造模,急性脑梗死 z-bio 2022-09-23 333

　　OBJECTIVE: To study the protective effect of Shenmai injection on brain tissue in mice with acute cerebral infarction and to preliminarily explore its possible mechanism.

　　Methods: In this experiment, 30 adult male CD-1 mice were used as the research objects, and they were randomly divided into control group, model group and experimental group, 10 mice in each group. The mouse model of acute cerebral infarction was constructed by suture method. The experimental group The mice in the control group and the model group were treated with 0.3 mL of Shenmai injection, and the control group and the model group were treated with the same dose of normal saline, and the erythrocyte function indexes of the mice in each group were compared. -PCR technique to detect the expression of calpain-1 and Bcl-2 in mouse cerebral cortex.

　　Results: Compared with the control group, the RBC-C3bR in the experimental group was significantly decreased, and the RBC-ICR was significantly increased (P<0.05). Compared with the model group, the RBC-C3bR in the experimental group was significantly increased, and the RBC-ICR was significantly decreased (P<0.05). . The number of TUNEL-positive cells in the brain tissue sections of the mice in the model group and experimental group was significantly higher than that in the control group (P<0.05); the number of TUNEL-positive cells in the brain tissue sections of the mice in the experimental group was significantly lower than that in the model group (P<0.05). ). Compared with the mice in the control group, the expression levels of calpain-1 protein and mRNA in the model group and experimental group were significantly increased, and the expression levels of Bcl-2 protein and mRNA were significantly decreased (P<0.05). Compared with the mice in the experimental group, the expression levels of calpain-1 protein and mRNA were significantly decreased, and the expression levels of Bcl-2 protein and mRNA were significantly increased (P<0.05).

　　Conclusion: Shenmai injection can improve erythrocyte function and inhibit neuronal apoptosis in mice with acute cerebral infarction. The possible mechanism is to down-regulate the expression of calpain-1 protein, up-regulate the expression of anti-apoptotic protein Bcl-2, and play the role of brain tissue neuron. Protective effects.