Objective: To observe the effect of berberine (BBR) on doxorubicin (DOX)-induced myocardial injury and its protective effect, and to further explore whether BBR can affect DOX-induced myocardial injury by regulating Wnt/β-catenin pathway. Methods: The rat myocardial cell line H9C2 was used as the research object and divided into Control group, model group, BBR group and LiCl agonist group. The cells in the control group were not treated. The DOX-induced myocardial injury model was established in the model group, BBR group and LiCl agonist group. The BBR group was intervened by BBR, and the LiCl agonist group was intervened by LiCl. CCK-8 method was used to detect the viability of cardiomyocytes. Flow cytometry was used to detect apoptosis. Western blot was used to detect the expression of Wnt/β-catenin pathway protein β-catenin, apoptosis-related proteins Bcl-2 and Bax. Results: (1)CCK-8 method : The cell viability of the model group was lower than that of the Control group (P<0.05), while the cell viability of the BBR group and the LiCl agonist group was higher than that of the model group (P<0.05). (2)Flow cytometry: The apoptosis rate of the model group was higher than that of the control group (P<0.05). The apoptosis rate of BBR group and LiCl agonist group was lower than that of model group (P<0.05). (3)Western blot: Compared with the Control group, the expression of Bax protein in the model group increased (P<0.05), the expression of Bcl-2 and β-catenin protein decreased (P<0.05), and the ratio of Bax/Bcl-2 also increased (P<0.05). Compared with the model group, the expression of Bax protein in BBR group and LiCl agonist group decreased (P<0.05), the expression of Bcl-2 protein increased (P<0.05), the expression of β-catenin protein increased (P<0.05), and the ratio of Bax/Bcl-2 decreased (P<0.05). Conclusion: BBR may play a protective role in cardiomyocytes by promoting the expression of β-catenin in damaged cardiomyocytes, up-regulating the activation of Wnt/β-catenin signaling pathway and inhibiting cardiomyocyte apoptosis.
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