Berberine inhibits the ischemia‑reperfusion injury induced inflammatory response and apoptosis of myocardial cells through the phosphoinositide 3‑kinase/RAC‑α serine/threonine‑protein kinase and nuclear factor-κB signaling pathways
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- Published online on: November 27, 2017 https://doi.org/10.3892/etm.2017.5575
- Pages: 1225-1232
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Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Myocardial ischemia‑reperfusion injury is one of the most common cardiovascular diseases, and can lead to serious damage and dysfunction of the myocardial tissue. Previous studies have demonstrated that berberine exhibits ameliorative effects on cardiovascular disease. The present study further investigated the efficacy and potential mechanism underlying the effects of berberine on ischemia‑reperfusion injury in a mouse model. Inflammatory markers were measured in the serum and levels of inflammatory proteins in myocardial cells were investigated after treatment with berberine. In addition, the apoptosis of myocardial cells was investigated after berberine treatment. Apoptosis‑associated gene expression levels and apoptotic signaling pathways were analyzed in myocardial cells after treatment with berberine. The phosphoinositide 3‑kinase (PI3K)/RAC‑α serine/threonine‑protein kinase (AKT) and nuclear factor (NF)‑κB signaling pathways were also analyzed in myocardial cells after treatment with berberine. Histological analysis was used to analyze the potential benefits of berberine in ischemia‑reperfusion injury. The present study identified that inflammatory responses and inflammatory factors were decreased in the myocardial cells of the mouse model of ischemia‑reperfusion injury. Mechanism analysis demonstrated that berberine inhibited apoptotic protease‑activating factor 1, caspase‑3 and caspase‑9 expression in myocardial cells. The expression of Bcl2‑associated agonist of cell death, Bcl‑2‑like protein 1 and cellular tumor antigen p53 was upregulated. Expression of NF‑κB p65, inhibitor of NF‑κB kinase subunit β (IKK‑β), NF‑κB inhibitor α (IκBα), and NF‑κB activity, were inhibited in myocardial cells in the mouse model of ischemia‑reperfusion injury. In conclusion, the results of the present study indicate that berberine inhibits inflammatory responses through the NF‑κB signaling pathway and suppresses the apoptosis of myocardial cells via the PI3K/AKT signaling pathway in a mouse model of ischemia‑reperfusion injury. These results suggest that berberine is a potential drug for the treatment of patients with ischemia‑reperfusion injury.
