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Ischemic heart disease is a leading cause of mortality and occurs due to coronary arterial atherosclerosis, vascular cavity stenosis and occlusion. It has previously been demonstrated that berberine treatment may ameliorate and help to prevent cardiovascular diseases due to its anti-inflammatory and anti-apoptotic effects in myocardial cells. However, the potential signaling mechanisms mediated by berberine in the progression of myocardial injury remain to be elucidated. The aim of the present study was to investigate the therapeutic effects of berberine and its potential mechanism in a mouse model of myocardial cell injury. The results revealed that berberine treatment downregulated the serum expression of inflammatory factors, including interleukin (IL)-6, tumor necrosis factor-α, IL-10 and IL-17A in mice with anoxia-reoxygenation injury. Berberine treatment also decreased myocardial cell apoptosis following anoxia-reoxygenation injury via regulating the expression of apoptosis-associated genes. Histological analysis revealed that the area, circumference fragmentation and segmentation of myocardial cells were significantly decreased by berberine treatment compared with the control group. The body weight, blood lipid levels, blood pressure and heart rate were markedly improved in mice with anoxia-reoxygenation injury following berberine treatment compared with untreated mice. The expression of p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB expression was downregulated in myocardial cells from in mice with anoxia-reoxygenation injury following berberine treatment compared with untreated mice. However, p38 MAPK overexpression ameliorated the berberine-induced decrease in NF-κB activity and expression, as well as the berberine-induced inhibition of myocardial apoptosis in myocardial cells isolated from experimental mice. In conclusion, the results of the present study indicate that berberine is able to decrease the expression of inflammatory cytokines expression and inhibit myocardial cell apoptosis via downregulating the p38 MAPK-mediated NF-κB signaling pathway. These results suggest that berberine may be an effective treatment for anoxia-reoxygenation injury.

Berberine protects myocardial cells against anoxia‑reoxygenation injury via p38 MAPK‑mediated NF‑κB signaling pathways