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Congenital heart disease (CHD) is a problem in the structure of the heart that is present at birth. Due to advances in interventional cardiology, CHD may currently be without surgery. The present study aimed to explore the molecular mechanism underlying CHD. A total of 200 cases of CHD treated by transcatheter closure as well as 200 controls were retrospectively assessed. Serum cytokines prior to and after treatment were assessed by reverse-transcription quantitative polymerase chain reaction analysis. Furthermore, the levels of proteins associated with c-Jun N-terminal kinase (JNK) and nuclear factor (NF)-κB were assessed by western blot analysis and immunohistochemistry. Furthermore, an animal model of CHD in young pigs was successfully constructed and treated with inhibitors of JNK and/or NF-κB to investigate the roles of these pathways in CHD. The results revealed that tumor necrosis factor-α, interleukin (IL)-6 and IL-8 were significantly elevated in the experimental group following transcatheter closure treatment, compared with those in the healthy control group, and the serum levels of the anti-inflammatory cytokine IL-10 were significantly reduced. Phosphorylated c-Jun and p65 levels in the experimental group were notably higher in the experimental group compared with the control group, but were restored to normal levels following transcatheter closure treatment. Similar results were also obtained in the pig model. The results of the present study suggested that the CHD-associated changes in cytokines, as well as their recovery following transcatheter closure treatment were associated with the JNK and NF-κB signaling pathways. The present study may provide further understanding of the underlying molecular mechanisms in CHD and propose a potential novel target for the treatment of CHD.

JNK and NF‑κB signaling pathways are involved in cytokine changes in patients with congenital heart disease prior to and after transcatheter closure