Objective: To study the protective effect of Shenmai injection on the brain tissue of 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 a control group, a model group and an experimental group, each with 10 mice. A mouse model of acute cerebral infarction was constructed by the thread plug method, the experimental group 0.3mL Shenmai injection was given. Both the control group and the model group were given the same dose of normal saline intervention, and the red blood cell function indexes of the mice in each group were compared. The TUNEL method was used to determine the neuronal apoptosis rate in brain tissue, and Western blot and q -PCR technology to detect the expression of calpain-1 and Bcl-2 in mouse brain cortex.
Results: Compared with the control group, the experimental group RBC-C3bR was significantly reduced, and RBC-ICR was significantly increased (P<0.05). Compared with the model group, the experimental group RBC-C3bR was significantly increased, and RBC-ICR was significantly decreased (P<0.05) 。 The number of TUNEL positive cells in the brain tissue sections of the model group and the experimental group was significantly higher than that of the control group (P<0.05); the number of TUNEL positive cells in the brain tissue section of the experimental group was significantly lower than that of the model group (P<0.05) ). Compared with mice in the control group, the expression levels of calpain-1 protein and mRNA in the model group and the experimental group increased significantly, and the expression levels of Bcl-2 protein and mRNA decreased significantly (P<0.05); compared with the model group mice In comparison, the expression levels of calpain-1 protein and mRNA in the experimental group mice were significantly reduced, and the expression levels of Bcl-2 protein and mRNA were significantly increased (P<0.05).
Conclusion: Shenmai injection can improve the red blood cell 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 exert brain tissue nerves. Protective effects.