Search

Background: Cardiac hypertrophy is characterized by an enlarged heart muscle, often due to increased workload or chronic heart diseases. Postn protein (periostin) plays a significant role in cardiac hypertrophy by influencing cardiomyocyte proliferation, inflammatory response, and fibrosis. The TGF-β and NF-κB pathways exacerbate inflammatory responses and structural changes in the heart during cardiac hypertrophy. Chlorogenic acid, found in plants, has antioxidant and anti-inflammatory properties, making it a potential candidate for inhibiting cardiac hypertrophy. Method: We used angiotensin II-induced H9c2 cardiomyocytes to construct a cell model of cardiac hypertrophy. Cells were categorized into control, model, shPostn, chlorogenic acid, and shPostn+chlorogenic acid groups. Various parameters, including cell surface area, activity, apoptosis rate, and expression levels of Postn, TGF-β/NF-κB pathway-related proteins, and mRNA, were evaluated. Results: Compared to the control group, the model group exhibited increased cell surface area and apoptosis rate, along with decreased cell activity. However, intervention with shPostn or chlorogenic acid led to significant reductions in cell surface area and apoptosis rate, coupled with increased cell viability. The shPostn+chlorogenic acid group showed further improvements. In addition, protein and mRNA expressions related to Postn, TGF-β/NF-κB pathways, and cardiac hypertrophy markers were upregulated in the model group but downregulated in the intervention groups, particularly the shPostn+chlorogenic acid group. Conclusion: Chlorogenic acid exerts its inhibitory effect on cardiac hypertrophy by modulating the TGF-β/NF-κB pathway through Postn protein. This study sheds light on potential therapeutic strategies for mitigating cardiac hypertrophy induced by angiotensin II and highlights chlorogenic acid as a promising candidate for further exploration in treating this condition.